Raynaud's affects parts of the body that have a characteristic circulatory pattern: a high density of direct connections between arterioles — small vessels that branch out from arteries — and venules, or small veins.
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Specifically within and between the pituitary lobes is anatomical evidence for confluent interlobe venules providing blood from the anterior to the neural lobe that would facilitate moment-to-moment sharing of information between lobes of the pituitary gland. In contrast to regular venules, high endothelial venules are a special type of venule where the endothelium is made up of simple cuboidal cells. Lymphocytes exit the blood stream and enter the lymph nodes via these specialized venules when an infection is detected. Compared with arterioles, the venules are larger with much weaker muscular coat.
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The bulbar conjunctival microvasculature contains arterioles, meta-arterioles, venules, capillaries, and communicating vessels. Vessel morphology varies greatly between subjects and even between regions of the individual eyes. In some subjects, arterioles and venules can be seen to run parallel with each other. Paired arterioles are generally smaller than corresponding venules.
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A venule is a very small blood vessel in the microcirculation that allows blood to return from the capillary beds to drain into the larger blood vessels, the veins. Venules range from 7μm to 1mm in diameter. Veins contain approximately 70% of total blood volume, 25% of which is contained in the venules. Many venules unite to form a vein.
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Salus's sign is a clinical sign in which deflection of retinal venules can be seen on fundoscopy occurring in patients with hypertensive retinopathy.Hypertension at Medscape Arteriosclerosis causes shortening or lengthening of arterioles, which causes venules to be moved at points where arterioles and venules cross over. This is seen at right-angle crossing points, where the venule crosses the arteriole in a horseshoe shape.Sebastian Wolf, Berndt Kirchof, Martin Reim.
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There are no large veins that drain blood away from the SA node. Instead, smaller venules drain the blood directly into the right atrium.
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It can be useful for controlling minor bleeding from capillaries and small venules, but ineffective and not indicated for massive or brisk arterial bleeding.
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Capillary blood, now deoxygenated, travels into venules and veins that ultimately collect in the superior and inferior vena cavae, and into the right heart.
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Some schistosome ova that are laid in intestinal and urinary venules backwash into the liver via the portal vein causing granuloma formation in the liver.
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The microcirculation is the circulation of the blood in the smallest blood vessels, the microvessels of the microvasculature present within organ tissues. The microvessels include terminal arterioles, metarterioles, capillaries, and venules. Arterioles carry oxygenated blood to the capillaries, and blood flows out of the capillaries through venules into veins. In addition to these blood vessels, the microcirculation also includes lymphatic capillaries and collecting ducts.
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These substances pass through capillaries through three different systems or mechanisms: diffusion, bulk flow, and transcytosis or vesicular transport. The liquid and solid exchanges that take place in the microvasculature particularly involve capillaries and post-capillary venules and collecting venules. Capillary walls allow the free flow of almost every substance in plasma. The plasma proteins are the only exception, as they are too big to pass through.
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GlyCAM-1 is expressed exclusively on high endothelial venules. It is unclear how GlyCAM-1 is attached to the membrane as it lacks a transmembrane region.
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Microvasculature is defined as the microvessels – venules and capillaries of the microcirculation, with a maximum average diameter of 0.3 millimeters."Microvascular" Merriam-Webster. N.p., n.d. Web. 21 May 2012.
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The vessels on the arterial side of the microcirculation are called the arterioles, which are well innervated, are surrounded by smooth muscle cells, and are 10-100 μm in diameter. Arterioles carry the blood to the capillaries, which are not innervated, have no smooth muscle, and are about 5-8 μm in diameter. Blood flows out of the capillaries into the venules, which have little smooth muscle and are 10-200 μm. The blood flows from the venules into the veins.
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Their function is to regulate blood flow before it enters the capillaries and venules by the contraction and relaxation of the smooth muscle found on their walls. The second sector is the capillary sector, which is represented by the capillaries, where substance and gas exchange between blood and interstitial fluid takes place. Finally, the post-capillary sector is represented by the post-capillary venules, which are formed by a layer of endothelial cells that allow free movement of some substances.
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The vasa recta of the kidney, (vasa rectae renis) are the straight arterioles, and the straight venules of the kidney, – a series of blood vessels in the blood supply of the kidney that enter the medulla as the straight arterioles, and leave the medulla to ascend to the cortex as the straight venules. (Latin: vasa, "vessels"; recta, "straight"). They lie parallel to the loop of Henle. These vessels branch off the efferent arterioles of juxtamedullary nephrons (those nephrons closest to the medulla).
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Venule walls have three layers: An inner endothelium composed of squamous endothelial cells that act as a membrane, a middle layer of muscle and elastic tissue and an outer layer of fibrous connective tissue. The middle layer is poorly developed so that venules have thinner walls than arterioles. They are porous so that fluid and blood cells can move easily from the bloodstream through their walls. Short portal venules between the neural and anterior pituitary lobes provide an avenue for rapid hormonal exchange via the blood.
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Their disposition can be alternate, opposite, or whorled (usually alternate except when subtending an inflorescence). Even, lamina keep entire and are setaceous or linear. The leaf just shows one vein without cross-venules. Stomata are not present.
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Metarterioles connect arterioles and capillaries. A tributary to the venules is known as a thoroughfare channel. The microcirculation has three major components: pre-capillary, capillary, and post-capillary. In the pre-capillary sector, arterioles, and precapillary sphincters participate.
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Some common dose-dependent adverse effects of amlodipine include vasodilatory effects, peripheral edema, dizziness, palpitations, and flushing. Peripheral edema (fluid accumulation in the tissues) occurs at rate of 10.8% at a 10-mg dose (versus 0.6% for placebos), and is three times more likely in women than in men. It causes more dilation in the arterioles and precapillary vessels than the postcapillary vessels and venules. The increased dilation allows for more blood, which is unable to push through to the relatively constricted postcapillary venules and vessels; the pressure causes much of the plasma to move into the interstitial space.
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Metarterioles exist in the mesenteric microcirculation, and the name was originally conceived only to define the "thoroughfare channels " between arterioles and venules. In recent times the term has often been used instead to describe the smallest arterioles directly prior to the capillaries.
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Br J Dermatol. 2003 Feb;148(2):342-5. The pathophysiology is still unclear, with most cases occurring sporadically, although rare cases were reported in families. Studies indicated the primary involvement of capillaries, venules and veins, and possibly also that of arterioles and lymphatics.
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Micrograph of cutaneous small-vessel vasculitis. The section shows all features of leucocytoclastic vasculitis. A mixed inflammatory cell population surrounding the postcapillary venules of the superficial dermis. The infiltrate consists of neutrophils with nuclear dust (dashed arrows) and shows high affinity for the vessels.
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Depletion of CD11c+ dendritic cells in mouse significantly altered the phenotype of HEV. The normal phenotype of HEV is possibly maintained by DC-secreted lymphotoxin (TNF-beta).Dendritic cells control lymphocyte entry to lymph nodes through high endothelial venules. Nature. 2011 Nov 13;479(7374):542-6.
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Changes in retinal blood circulation are seen with aging and exposure to air pollution, and may indicate cardiovascular diseases such as hypertension and atherosclerosis. Determining the equivalent width of arterioles and venules near the optic disc is also a widely used technique to identify cardiovascular risks.
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After the oxygen is removed blood reaches venules and later veins which will take it back to the heart and lungs. On the other hand, when there is an AVM blood goes directly from arteries to veins through the abnormal vessels disrupting the normal circulation of blood.
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The sporozoites are then carried by the circulation of the hemolymph to the salivary glands, where they become concentrated in the acinal cells. A small number of sporozoites are introduced into the salivary duct and injected into the venules of the bitten human. This initiates the cycle in the human liver.
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The arterioles supply capillaries, which in turn empty into venules. The first branches off of the aorta are the coronary arteries, which supply blood to the heart muscle itself. These follow by the branches of the aortic arch, namely the brachiocephalic artery, the left common carotid, and the left subclavian arteries.
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Capillaries merge into venules, which merge into veins. The venous system feeds into the two major veins: the superior vena cava - which mainly drains tissues above the heart - and the inferior vena cava - which mainly drains tissues below the heart. These two large veins empty into the right atrium of the heart.
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Typically, vSMCs wrap around larger vessels: they form a dense continuum spindling around arteries, arterioles and precapillary arterioles; while around postcapillary venules, vSMCs adopt a different morphology: individual cell bodies extending thing branching processes, that become more stellate-like around venules and veins. The cell body of pericytes has a round shape extending a few processes in a longitudinal fashion along the capillaries. Recently, efforts have been undertaken using single cell sequencing on mural cells to try to characterize their molecular signature along the blood vessels. This showed that there is a zonation in their expression patterns by which they can be grouped into different subsets, but no singular markers have been found so far that can identify unequivocally any of the cell types.
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Infections happen when a human swallows water or food contaminated with unhatched eggs, which hatch into juveniles in the duodenum. Then they penetrate the mucosa and submucosa and enter venules or lymphatics. Next, they pass through the right heart and into pulmonary circulation. They then break out of the capillaries and enter the air spaces.
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Microangiopathy (or microvascular disease, or small vessel disease) is an angiopathy (i.e. disease of blood vessels) affecting small blood vessels in the body. It can be contrasted to macroangiopathy, or large vessel disease. Cerebral small vessel disease refers to a group of diseases that affect the small arteries, arterioles, venules, and capillaries of the brain.
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Diabetic retinopathy, which can develop into proliferative diabetic retinopathy, is a condition where capillaries in the retina become occluded, which creates areas of ischemic retina and triggering the release of angiogenic growth factors. This retinal ischemia stimulates the proliferation of new blood vessels from pre-existing retinal venules. It is the leading cause of blindness of working age adults.
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Commonly affected zones name="JAmAcadDermatol2004-Wilkin"> Micrograph showing rosacea as enlarged, dilated capillaries and venules located in the upper dermis, angulated telangiectasias, perivascular and perifollicular lymphocytic infiltration, and superficial dermal edema. Four rosacea subtypes exist, and a patient may have more than one subtype:Marks, James G; Miller, Jeffery (2006). Lookingbill and Marks' Principles of Dermatology (4th ed.). Elsevier Inc. .
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An adenomere is the functional unit in a developing gland. The glands include the salivary and lacrimal glands. Adenomeres are secretory sublobular units having a centrally located collecting duct that connects with postcapillary venules; and is a structural-functional unit in the gland. They consist of all the secretory cells that release their products into a single intralobular duct.
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The precise mechanism of acrocyanosis is not known. The current line of thinking goes that vasospasms in the cutaneous arteries and arterioles produce cyanotic discoloration, while compensatory dilatation in the postcapillary venules causes sweating. Arteriovenous subpapillary plexus shunting also occurs. Persistent vasoconstriction at the precapillary sphincter creates a local hypoxic environment, thus releasing adenosine into the capillary bed.
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The thin-walled venules are compressed and the resistance to flow in these vessels increases. This is accompanied with a decrease in blood flow causing an aggregation of red blood cells and subsequent increase in blood viscosity. This tissue also becomes ischaemic which suppresses the cellular metabolism in the area of the pulp that is affected. This causes necrosis.
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Antigen-presenting cells accumulate near high endothelial venules to process soluble antigens. Antigens are also presented on the surface of dendritic cells. In an inflammatory state, lymphatic endothelial cells increase their surface adhesion molecules, and dendritic cells express a surface CCR7 receptor. This type of receptor interacts with the chemokine CCL21, produced by fibroblastic reticular cells.
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Very little is known about the pathology of Hashimoto's encephalopathy. Post mortem studies of some individuals have shown lymphocytic vasculitis of venules and veins in the brain stem and a diffuse gliosis involving gray matter more than white matter. As mentioned above, autoantibodies to alpha-enolase associated with Hashimoto's encephalopathy have thus far been the most hypothesized mechanism of injury.
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Power Doppler is a Doppler sequence that measures the ultrasonic energy backscattered from red blood cells in each pixel of the image. It provides no information on blood velocity but is proportional to blood volume within the pixel. However, conventional power Doppler imaging lacks sensitivity to detect small arterioles/venules and thus is unable to provide local neurofunctional information through neurovascular coupling.
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The superior and inferior venae cavae carry relatively deoxygenated blood from the upper and lower systemic circulations, respectively. The portal venous system is a series of veins or venules that directly connect two capillary beds. Examples of such systems include the hepatic portal vein and hypophyseal portal system. The peripheral veins carry blood from the limbs and hands and feet.
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Diagram of the circulation related to a single glomerulus, associated tubule, and collecting system. The glomerulus receives its blood supply from an afferent arteriole of the renal arterial circulation. Unlike most capillary beds, the glomerular capillaries exit into efferent arterioles rather than venules. The resistance of the efferent arterioles causes sufficient hydrostatic pressure within the glomerulus to provide the force for ultrafiltration.
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Addressin also known as mucosal vascular addressin cell adhesion molecule 1 (MAdCAM-1) is a protein that in humans is encoded by the MADCAM1 gene. Addressin is an extracellular protein of the endothelium of venules. Addressins are the ligands to the homing receptors of lymphocytes.Addressin at eMedicine Dictionary The task of these ligands and their receptors is to determine which tissue the lymphocyte will enter next.
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In order to maintain pressure, the capillaries branch off to a web of vessels that carry blood into the venules. Through this process blood undergoes micro-circulation. In micro- circulation, the Fåhræus effect will take place, resulting in a large change in hematocrit. As blood flows through the arterioles, red cells will act a feed hematocrit (Hf), while in the capillaries, a tube hematocrit (Ht) occurs.
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Thy1 expression varies between species. Amongst the cells reported to generally express Thy-1 are thymocytes (precursor of T cells in the thymus) & CD34(+) prothymocytes; neurons, mesenchymal stem cells, hematopoietic stem cells, NK cells, murine T-cells, endothelium (mainly in high endothelial venules or HEVs where diapedesis takes place), renal glomerular mesangial cells, circulating metastatic melanoma cells, follicular dendritic cells (FDC), a fraction of fibroblasts and myofibroblasts.
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Interleukin 33 (IL-33) is a cytokine belonging to the IL-1 superfamily. IL-33 induces helper T cells, mast cells, eosinophils and basophils to produce type 2 cytokines. This cytokine was previously named NF-HEV 'nuclear factor (NF) in high endothelial venules' (HEVs) since it was originally identified in these specialized cells. IL-33 acts intracellularly as a nuclear factor and extracellularly as a cytokine.
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Goldberg classified PSR into following 5 different self-explanatory stages: # Stage of peripheral arterial occlusion and ischemia: It is the earliest abnormality that can be visualized by fundus examination. The occluded arterioles can be seen as dark red lines. They eventually turn into white silver-wire vessels. # Stage of peripheral arteriolar-venular anastomoses: Arteriolar-venular anastomoses develop as blood is diverted from blocked arteries to nearby venules.
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They may be composed of abnormal aggregations of arterioles, capillaries or venules. Because telangiectasias are vascular lesions, they blanch when tested with diascopy. Telangiectasias, aside from presenting in many other conditions, are one of the features of the acronymically named CREST syndrome, a form of systemic scleroderma. The syndrome recognises the significantly co-presenting symptoms of calcinosis, Raynaud's phenomenon, esophageal dysmotility, sclerodactyly and telangiectasia.
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Portal venous systems are considered venous because the blood vessels that join the two capillary beds are either veins or venules. Examples of such systems include the hepatic portal system, the hypophyseal portal system, and (in non-mammals) the renal portal system. Unqualified, portal venous system often refers to the hepatic portal system. For this reason, portal vein most commonly refers to the hepatic portal vein.
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Nerves connect the spinal cord and brain to the rest of the body. All major bones, muscles, and nerves in the body are named, with the exception of anatomical variations such as sesamoid bones and accessory muscles. Blood vessels carry blood throughout the body, which moves because of the beating of the heart. Venules and veins collect blood low in oxygen from tissues throughout the body.
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Figure 2: Adrenal blood flow. Adrenal gland is vulnerable to hemorrhage due to its special vascular supply. It has rich blood supply via 50 to 60 small arterial branches from three adrenal arteries. The branches then form a sub-capsular plexus within the adrenal cortex, which drains into medullary sinusoids through relatively fewer venules and flows into a single vein, creating a potential “vascular dam”.
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The process is highly regulated by cell adhesion molecules, particularly, the addressin also known as MADCAM1. This antigen is known for its role in tissue- specific adhesion of lymphocytes to high endothelium venules. Through these interactions they play a crucial role in orchestrating circulating lymphocytes. CAM function in cancer metastasis, inflammation, and thrombosis makes it a viable therapeutic target that is currently being considered.
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The glomerulus receives its blood supply from an afferent arteriole of the renal arterial circulation. Unlike most capillary beds, the glomerular capillaries exit into efferent arterioles rather than venules. The resistance of the efferent arterioles causes sufficient hydrostatic pressure within the glomerulus to provide the force for ultrafiltration. The glomerulus and its surrounding Bowman's capsule constitute a renal corpuscle, the basic filtration unit of the kidney.
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Interactions between stromal and hematopoietic cells are important for the development of lymph nodes. Crosstalk LEC, lymphoid tissue inducer cells and mesenchymal stromal organizer cells initiate the formation of lymph nodes. Naive lymphocytes (those with no history of contact with antigens) travel from the bone marrow or high endothelial venules of the thymus where they develop as lymphoblasts, to lymph nodes, where they mature.
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It also creates a porous molecular sieve in the lymph node. The lymph carries chemokines (molecular chemical messengers) and antigens to the lymph node. At the lymph node, the lymph passes quickly through the reticular network to the T cell zone and the high endothelial venules. FRCs express chemokines such as CCL21 and CCL19 which assist the movement of T cells and dendritic cells with CCR7 receptors.
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In tube hematocrit, plasma fills most of the vessel while the red cells travel through in somewhat of a single file line. From this stage, blood will enter the venules increasing in hematocrit, in other words the discharge hematocrit (Hd).In large vessels with low hematocrit, viscosity dramatically drops and red cells take in a lot of energy. While in smaller vessels at the micro- circulation scale, viscosity is very high.
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Normal vision The same view with diabetic retinopathy. Emptied retinal venules due to arterial branch occlusion in diabetic retinopathy (fluorescein angiography) Diabetic retinopathy often has no early warning signs. Even macular edema, which can cause rapid vision loss, may not have any warning signs for some time. In general, however, a person with macular edema is likely to have blurred vision, making it hard to do things like read or drive.
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Capillaries are organized into capillary beds in tissues; it is here that blood exchanges oxygen for carbon dioxide waste. In the capillary beds, blood flow is slowed to allow maximum diffusion of oxygen into the tissues. Once the blood has become deoxygenated, it travels through venules then veins and back to the heart. Veins, unlike arteries, are thin and rigid as they do not need to withstand extreme pressure.
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The limited venous drainage builds the blood flow resistance and adrenal venous pressure, resulting in the hemorrhage into the gland. Under physiological stress, ACTH and catecholamine secretion increases, which further promotes adrenal arterial blood flow. Increased catecholamine level constricts the venules and enhances platelet aggregation, which may induce adrenal vein thrombosis. The synergistical effect builds up pressure within the venous sinusoids, predisposing to adrenal gland congestion and venous stasis.
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Capillaries are organized into capillary beds in tissues, it is here that blood exchanges oxygen for carbon dioxide waste. In the capillary beds blood flow is slowed to allow maximum diffusion of oxygen into the tissues. Once the blood has become deoxygenated it travels through venules then veins and back to the heart. Veins, unlike arteries, are thin and rigid as they do not need to withstand extreme pressure.
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MadCam-1 receptor MadCAM-1 expression is continuous in the high endothelial venules of Peyer's patches and in the micro-vessels of the intestinal tract. MadCAM-1 inhibitors prevent T cell migration to the gut. Structural analysis of the MadCAM-1 protein shows that it is a 41.5 kDa transmembrane protein with a small cytoplasmic tail and a large extracellular region. This extracellular region includes three immunoglobin-like (Ig) domains.
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High endothelial venules (HEV) are specialized post-capillary venous swellings characterized by plump endothelial cells as opposed to the usual thinner endothelial cells found in regular venules. HEVs enable lymphocytes circulating in the blood to directly enter a lymph node (by crossing through the HEV). Table 14-1 In humans, HEVs are found in all secondary lymphoid organs (with the exception of spleen, where blood exits through open arterioles and enters the red pulp), including hundreds of lymph nodes dispersed in the body, tonsils and adenoids in the pharynx, Peyer's patches (PIs) in the small intestine, appendix, and small aggregates of lymphoid tissue in the stomach and large intestine. In contrast to the endothelial cells from other vessels, the high endothelial cells of HEVs have a distinctive appearance, consisting of a cuboidal morphology and with various receptors to interact with leukocytes (express specialized ligands for lymphocytes and are able to support high levels of lymphocyte extravasation).
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Angioimmunoblastic T-cell lymphoma (AITL) is a fast-growing form of mature T-cell lymphoma, accounting for 18.5% of patients. It is characterised by systemic disorders, polymorphous lymphoid infiltrate and a significant increase in proliferation of follicular dendritic cells and high endothelial venules. It originates from follicular T helper (TFH) cells, which is important in maintaining immune response. Autoimmune disorders like lymphopenia and hypergammaglobulinemia can be observed in about 50% patients with AITL.
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As a result of its breakdown to nitric oxide (NO), sodium nitroprusside has potent vasodilating effects on arterioles and venules (veins more than arteries) but this selectivity is much less marked than that of nitroglycerin. Sodium nitroprusside breaks down in circulation to release nitric oxide (NO). It does this by binding to oxyhaemoglobin to release cyanide, methaemoglobin and nitric oxide. NO activates guanylate cyclase in vascular smooth muscle and increases intracellular production of cGMP.
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This induces gas and nutrients to move from the blood to the cells, due to the lower osmotic pressure outside the capillary. The opposite process occurs when the blood leaves the capillaries and enters the venules, where the blood pressure drops due to an increase in flow rate. Arterioles receive autonomic nervous system innervation and respond to various circulating hormones in order to regulate their diameter. Retinal vessels lack a functional sympathetic innervation.
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The organism goes through asexual reproduction phase that is called schizogony which occurs in the mononuclear phagocytic cells. In the tissue phase the macrophage cells that are infected often clog venules in organs such as the liver, spleen, lungs, and lymph nodes. It is this phase that is associated with clinical disease if the schizonts are numerous. Schizonts next form merozoites that break out of the macrophage cells and infect the red blood cells (erythrocytes).
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Guyton, A.C. & Hall, J.E. (2006) Textbook of Medical Physiology (11th ed.) Philadelphia: Elsevier Saunder Vasospasms force adenosine to enter the capillary bed, where it vasodilates the postcapillary venules. Such differences in vessel tone create a countercurrent exchange system that attempts to retain heat. Profuse sweating would then be caused by an overwhelmed countercurrent exchange system. In addition to adenosine, other hormones may contribute to acrocyanosis such as increase blood levels of serotonin.
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Lymphatic capillaries are slightly larger in diameter than blood capillaries, and have closed ends (unlike the blood capillaries open at one end to the arterioles and open at the other end to the venules). This structure permits interstitial fluid to flow into them but not out. Lymph capillaries have a greater internal oncotic pressure than blood capillaries, due to the greater concentration of plasma proteins in the lymph.Guyton, Arthur; Hall, John (2006).
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Each arcuate artery supplies several interlobular arteries that feed into the afferent arterioles that supply the glomeruli. After filtration occurs, the blood moves through a small network of venules that converge into interlobular veins. As with the arteriole distribution, the veins follow the same pattern: the interlobular provide blood to the arcuate veins then back to the interlobar veins, which come to form the renal vein exiting the kidney for transfusion for blood.
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While N. americanus larvae only infect through penetration of skin, A. duodenale can infect both through penetration and orally. After the L3 larvae have successfully entered the host, they then travel through the subcutaneous venules and lymphatic vessels of the human host. Eventually, the L3 larvae enter the lungs through the pulmonary capillaries and break out into the alveoli. They then travel up the trachea to be coughed and swallowed by the host.
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Cutaneous small-vessel vasculitis (CSVV), also known as hypersensitivity vasculitis, cutaneous leukocytoclastic vasculitis, hypersensitivity angiitis, cutaneous leukocytoclastic angiitis, cutaneous necrotizing vasculitis and cutaneous necrotizing venulitis, is inflammation of small blood vessels (usually post-capillary venules in the dermis), characterized by palpable purpura. It is the most common vasculitis seen in clinical practice. "Leukocytoclastic" refers to the damage caused by nuclear debris from infiltrating neutrophils in and around the vessels.Harrison's Principles of Internal Medicine.
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These cells have characteristic positions, with alpha cells (secreting glucagon) tending to be situated around the periphery of the islet, and beta cells (secreting insulin) more numerous and found throughout the islet. Enterochromaffin cells are also scattered throughout the islets. Islets are composed of up to 3,000 secretory cells, and contain several small arterioles to receive blood, and venules that allow the hormones secreted by the cells to enter the systemic circulation.
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Congestive hepatopathy, is liver dysfunction due to venous congestion, usually due to congestive heart failure. The gross pathological appearance of a liver affected by chronic passive congestion is "speckled" like a grated nutmeg kernel; the dark spots represent the dilated and congested hepatic venules and small hepatic veins. The paler areas are unaffected surrounding liver tissue. When severe and longstanding, hepatic congestion can lead to fibrosis; if congestion is due to right heart failure, it is called cardiac cirrhosis.
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In a healthy vascular system the endothelium lines all blood-contacting surfaces, including arteries, arterioles, veins, venules, capillaries, and heart chambers. This healthy condition is promoted by the ample production of nitric oxide by the endothelium, which requires a biochemical reaction regulated by a complex balance of polyphenols, various nitric oxide synthase enzymes and L-arginine. In addition there is direct electrical and chemical communication via gap junctions between the endothelial cells and the vascular smooth muscle.
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The region of the lymph node called the paracortex immediately surrounds the medulla. Unlike the cortex, which has mostly immature T cells, or thymocytes, the paracortex has a mixture of immature and mature T cells. Lymphocytes enter the lymph nodes through specialised high endothelial venules found in the paracortex. A lymph follicle is a dense collection of lymphocytes, the number, size, and configuration of which change in accordance with the functional state of the lymph node.
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Blood vessels function to transport blood. In general, arteries and arterioles transport oxygenated blood from the lungs to the body and its organs, and veins and venules transport deoxygenated blood from the body to the lungs. Blood vessels also circulate blood throughout the circulatory system Oxygen (bound to hemoglobin in red blood cells) is the most critical nutrient carried by the blood. In all arteries apart from the pulmonary artery, hemoglobin is highly saturated (95–100%) with oxygen.
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The Heart, arteries, and veins (a network of tubes to carry blood) constitute the cardiovascular system or circulatory system of our body which transports the blood throughout the body. The heart can be thought of as a muscular pump, consisting of four chambers, and pulsatile muscles which pump and circulates the blood through the vasculature. Arteries, arterioles, capillaries, venules, and veins make up the vasculature. The cardiovascular system circulates about 5 liters of blood at a rate of approximately 6 l/m.
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Each arcuate artery supplies several interlobular arteries that feed into the afferent arterioles that supply the glomeruli. Blood drains from the kidneys, ultimately into the inferior vena cava. After filtration occurs, the blood moves through a small network of small veins (venules) that converge into interlobular veins. As with the arteriole distribution, the veins follow the same pattern: the interlobular provide blood to the arcuate veins then back to the interlobar veins, which come to form the renal veins which exiting the kidney .
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Glycosylation-dependent cell adhesion molecule-1 (GLYCAM1) is a proteoglycan ligand expressed on cells of the high endothelial venules in lymphoid tissues. It is the ligand for the receptor L-selectin allowing for naive lymphocytes to exit the bloodstream into lymphoid tissues. GLYCAM1 binds to L-selectin by presenting one or more O-linked carbohydrates to the lectin domain of the leukocyte cell surface selectin. Data suggests that GLYCAM1 is a hormone- regulated milk protein that is part of the milk mucin complex.
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A capillary is a small blood vessel from 5 to 10 micrometres (μm) in diameter, and having a wall one endothelial cell thick. They are the smallest blood vessels in the body: they convey blood between the arterioles and venules. These microvessels are the site of exchange of many substances with the interstitial fluid surrounding them. Substances which exit include water (proximal portion), oxygen, and glucose; substances which enter include water (distal portion), carbon dioxide, uric acid, lactic acid, urea and creatinine.
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Merozoites emerge from the second-generation meronts and enter the mononucleated cells, where they develop by endodyogeny. Subsequent generations of merozoites develop downstream in the direction of blood flow to arterioles, capillaries, venules, and veins throughout the body, subsequently developing into the final asexual generation in muscles. Merozoites entering muscle cells round up to form metrocytes and initiate sarcocyst formation. Sarcocysts begin as unicellular bodies containing a single metrocyte and through asexual multiplication numerous metrocytes accumulate and the sarcocyst increases in size.
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L-selectin acts as a "homing receptor" for lymphocytes to enter secondary lymphoid tissues via high endothelial venules. Ligands present on endothelial cells will bind to lymphocytes expressing L-selectin, slowing lymphocyte trafficking through the blood, and facilitating entry into a secondary lymphoid organ at that point. The receptor is commonly found on the cell surfaces of T cells. Naive T-lymphocytes, which have not yet encountered their specific antigen, need to enter secondary lymph nodes to encounter their antigen.
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Survivors enter the liver within 24 hours. From the liver they enter the portal vein to reach different parts of the body. Unlike other species again, the schistosomulae of S. haematobium reach the vesical vessels through anastomotic channels between radicles of the inferior mesenteric vein and pelvic veins. After living inside small venules in the submucosa and wall of the bladder, they migrate to the perivesical venous plexus (a group of veins at the lower portion of the bladder) to attain full maturation.
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The vascular amyloid pathology characteristic of CAA can be classified as either Type 1 or Type 2, the latter type being the more common. Type 1 CAA pathology entails detectable amyloid deposits within cortical capillaries as well as within the leptomeningeal and cortical arteries and arterioles. In type 2 CAA pathology, amyloid deposits are present in leptomeningeal and cortical arteries and arterioles, but not in capillaries. Deposits in veins or venules are possible in either type but are far less prevalent.
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The splenic vein is formed from small venules that leave the spleen. It travels above the pancreas, alongside the splenic artery. It collects branches from the stomach and pancreas, and most notably from the large intestine (also drained by the superior mesenteric vein) via the inferior mesenteric vein, which drains in the splenic vein shortly before the origin of the hepatic portal vein. The splenic vein ends in the portal vein, formed when the splenic vein joins the superior mesenteric vein.
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High endothelial cells (HECs) are specialized vascular endothelial cells. In the thymus, they line the high endothelial venules (HEVs) where lymphocytes originate. The HEVs of the lymph node express adhesion molecules like peripheral node addressin (PNAd) that are essential for the migration of naive T cells from the peripheral blood to the lymph node. In mouse lymph nodes the HECs also express the chemokine CCL21 which will bind its recpeptor CCR7 on the naive T-cell and enhance the migration.
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Filariform larvae can survive for up to two weeks, they are extremely motile and will move onto higher ground to improve their chances of finding a host. N. americanus larvae can only infect through penetrating skin, but A. duodenale can also infect orally. A common route of passage for the larvae is the skin of barefoot walkers. Once the larvae have entered the host they travel in the circulatory system to the lungs where they leave the venules and enter the alveoli.
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Angiogenesis is the most common type of neovascularization seen in development and growth, and is import to both physiological and pathological processes. Angiogenesis occurs through the formation of new vessels from pre-existing vessels. This occurs through the sprouting of new capillaries from post-capillary venules, requiring precise coordination of multiple steps and the participation and communication of multiple cell types. The complex process is initiated in response to local tissue ischemia or hypoxia, leading to the release of angiogenic factors such as VEGF and HIF-1.
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The medulla contains plasma cells, as well as macrophages which are present within the medullary sinuses. As part of the reticular network, there are follicular dendritic cells in the B cell follicle and fibroblastic reticular cells in the T cell cortex. The reticular network provides structural support and a surface for adhesion of the dendritic cells, macrophages and lymphocytes. It also allows exchange of material with blood through the high endothelial venules and provides the growth and regulatory factors necessary for activation and maturation of immune cells.
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Dilated capillaries may also be noted within this area, and while this is often difficult to visualize ophthalmoscopically, the abnormal capillary pattern is readily identifiable with fluorescein angiography. Areas of focal RPE hyperplasia, i.e., pigment plaques, often develop in the paramacular region as a response to these abnormal vessels. Other signs of macular telangiectasia type 2 include right angle venules, representing an unusual alteration of the vasculature in the paramacular area, with vessels taking an abrupt turn toward the macula as if being dragged.
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Myocardium itself is well vascularized, with highly branched arterioles and venules, as well as a high degree of capillarization. Major arteries and veins run longitudinally to and from the red swimming muscles, which are found close to the spinal column, just underneath the skin. Small arteries branch off and penetrate the red muscle, delivering oxygenated blood, whereas veins take deoxygenated blood back to the heart. The red muscles also have a high myoglobin content and capillary density, where many of the capillaries branch off.
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They enter the medulla, and surround the loop of Henle. Whereas the peritubular capillaries surround the cortical parts of the tubules, the vasa recta go into the medulla and are closer to the loop of Henle, and leave to ascend to the cortex. Terminations of the vasa recta form the straight venules, branches from the plexuses at the apices of the medullary pyramids. They run outward in a straight course between the tubes of the medullary substance and join the interlobular veins to form venous arcades.
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Naive lymphocytes are able to circulate into secondary lymphoid tissues, Peyer’s patches, lymph nodes, and the spleen. Because they have not yet been exposed to antigen, these lymphocytes are undifferentiated and express few homing receptors. High endothelial venules (HEVs) are cells found in secondary lymphoid organs that express large quantities of cell adhesion molecules, enabling undifferentiated lymphocytes to bind. After entering lymph nodes and Peyer’s patches via HEVs, naive T and B cells are exposed to antigen circulating in lymph and differentiate to contribute to the adaptive immune response.
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The central veins of liver (or central venules) are veins found at the center of hepatic lobules (one vein at each lobule center). They receive the blood mixed in the liver sinusoids and return it to circulation via the hepatic veins. The Circulation of venous blood is: Portal vein (which is formed by the joining of the superior mesenteric vein with the splenic vein) drains into the sinusoids of the liver, these all drain into the central veins of liver which drain into the hepatic vein to be returned to IVC.
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Despite intensive efforts, few HEV-specific markers have been described. The best HEV marker currently available is a carbohydrate epitope recognized by the monoclonal antibody (mAb) MECA-79, which stains all HEVs within lymphoid tissues and does not react with postcapillary venules or large vessels in spleen, thymus or nonlymphoid tissues. MECA-79 mAb inhibits lymphocyte emigration through HEVs into lymph nodes in vivo and lymphocyte adhesion to lymph node and tonsil HEVs in vitro. Although initially produced against mouse HEVs, the mAb shows a wide crossreactivity among species.
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There are five types of blood vessels: the arteries, which carry the blood away from the heart; the arterioles; the capillaries, where the exchange of water and chemicals between the blood and the tissues occurs; the venules; and the veins, which carry blood from the capillaries back towards the heart. The word vascular, meaning relating to the blood vessels, is derived from the Latin vas, meaning vessel. Some structures – such as cartilage, the epithelium, and the lens and cornea of the eye – do not contain blood vessels and are labeled avascular.
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Pericytes (previously known as Rouget cells) are multi-functional mural cells of the microcirculation that wrap around the endothelial cells that line the capillaries and venules throughout the body. Pericytes are embedded in basement membrane, where they communicate with endothelial cells of the body's smallest blood vessels by means of both direct physical contact and paracrine signaling. Pericytes help to maintain homeostatic and hemostatic functions in the brain and also sustain the blood–brain barrier. These cells are also a key component of the neurovascular unit, which includes endothelial cells, astrocytes, and neurons.
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It has also been found in Namibian ostriches and other desert birds, where a buildup of salt concentration is due to dehydration and scarcity of drinking water. In seabirds the salt gland is above the beak, leading to a main canal above the beak, and water is blown from two small nostrils on the beak, to empty it. The salt gland has two countercurrent mechanisms working in it: a. A salt extraction system with a countercurrent multiplication mechanism, where salt is actively pumped from the blood 'venules' (small veins) into the gland tubules.
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Diagram of a capillary Blood flows from the heart through arteries, which branch and narrow into arterioles, and then branch further into capillaries where nutrients and wastes are exchanged. The capillaries then join and widen to become venules, which in turn widen and converge to become veins, which then return blood back to the heart through the venae cavae. In the mesentery, metarterioles form an additional stage between arterioles and capillaries. Individual capillaries are part of the capillary bed, an interweaving network of capillaries supplying tissues and organs.
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The more metabolically active a tissue is, the more capillaries are required to supply nutrients and carry away products of metabolism. There are two types of capillaries: true capillaries, which branch from arterioles and provide exchange between tissue and the capillary blood, and sinusoids, a type of open-pore capillary found in the liver, bone marrow, anterior pituitary gland, and brain circumventricular organs. Capillaries and sinusoids are short vessels that directly connect the arterioles and venules at opposite ends of the beds. Metarterioles are found primarily in the mesenteric microcirculation.
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Posterior abdominal wall, after removal of the peritoneum, showing kidneys, suprarenal capsules, and great vessels. (Hepatic veins labeled at center top.) Any obstruction of the venous vasculature of the liver is referred to as Budd–Chiari syndrome, from the venules to the right atrium. This leads to increased portal vein and hepatic sinusoid pressures as the blood flow stagnates. The increased portal pressure causes increased filtration of vascular fluid with the formation of ascites in the abdomen and collateral venous flow through alternative veins leading to esophageal, gastric and rectal varices.
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Veins serve to return blood from organs to the heart. Veins are also called "capacitance vessels" because most of the blood volume (60%) is contained within veins. In systemic circulation oxygenated blood is pumped by the left ventricle through the arteries to the muscles and organs of the body, where its nutrients and gases are exchanged at capillaries. After taking up cellular waste and carbon dioxide in capillaries, blood is channeled through vessels that converge with one another to form venules, which continue to converge and form the larger veins.
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Blood exits the glomerular capillaries by an efferent arteriole instead of a venule, as is seen in the majority of capillary systems (Fig. 4). This provides tighter control over the blood flow through the glomerulus, since arterioles dilate and constrict more readily than venules, owing to their thick circular smooth muscle layer (tunica media). The blood exiting the efferent arteriole enters a renal venule, which in turn enters a renal interlobular vein and then into the renal vein. Cortical nephrons near the corticomedullary junction (15% of all nephrons) are called juxtamedullary nephrons.
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ANTU is specifically toxic in lung cells due to its conversion to a short-lived active metabolite to which it is converted in the liver, not ANTU acting directly. This damage is focused on the endothelium of pulmonary capillaries and venules, it will lead to the formation of irreversible gaps in the endothelium of pulmonary vessels. This damage can lead to pulmonary edema. In ANTU poisoning plasma, carbon and ferritin escape through a gap in the thick part of the pulmonary capillary into the interstitial tissues of the lungCunningham, A. L., and J. V. Hurley.
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After capillaries, the blood enters the venules before joining smaller veins first and then larger veins before reaching the right heart. Thus completing the cycle of blood going to heart and then coming from it and going to all parts of the body."Bio-Fluid Dynamics, P.Nithiarasu" The tricuspid valve, right heart (right ventricle), pulmonary valve, pulmonary artery, lungs, pulmonary veins and right heart are the elements of the Pulmonary Circulation System. The process of gas exchange, that is, exchange of carbon dioxide with oxygen in the lungs is the main function of the pulmonary system.
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The interaction of the α4β7 integrin and the addressin (also known as MADCAM1) endothelial cell receptor is believed to contribute to the chronic bowel inflammation that causes Crohn's disease. Addressin is primarily expressed in the endothelium of venules in the small intestine and are critical in guiding T-lymphocytes to lymphatic tissues in Peyer's patches. In CD patients, sites of active inflammation of the bowel in CD patients have increased expression of addressin, suggesting a connection between the inflammation and the receptor. Natalizumab may block interaction between the α4β7 integrin and addressin at sites of inflammation.
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Henoch–Schönlein purpura is a small-vessel vasculitis in which complexes of immunoglobulin A (IgA) and complement component 3 (C3) are deposited on arterioles, capillaries, and venules (hence it is a type III hypersensitivity reaction). As with IgA nephropathy, serum levels of IgA are high in HSP and there are identical findings on renal biopsy; however, IgA nephropathy has a predilection for young adults while HSP is more predominant among children. Further, IgA nephropathy typically only affects the kidneys while HSP is a systemic disease. HSP involves the skin and connective tissues, scrotum, joints, gastrointestinal tract and kidneys.
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Laboratory tests commonly reveal the presence of immune-mediated hemolytic anemia; elevated blood levels of eosinophils, gamma globulins, and lactic dehydrogenase; high erythrocyte sedimentation rates; and positive blood tests for autoantibodies such as rheumatoid factor, anti-nuclear antibody, and anti-smooth muscle antibody. Several of these clinical and laboratory features suggest that the afflicted individuals have an underlining abnormality in their immune system. Involved tissues exhibit vascular proliferation, small lymphoid cells clustered around venules in a background containing TFH cells, activated lymphocytes, follicular dendritic cells, epithelioid cells, plasma cells, and eosinophils. Only the TFH cells are malignant.
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On penetration, the head of the cercaria transforms into an endoparasitic larva, the schistosomule. Each schistosomule spends a few days in the skin and then enters the circulation starting at the dermal lymphatics and venules. Here, they feed on blood, regurgitating the haem as hemozoin. The schistosomule migrates to the lungs (5–7 days post-penetration) and then moves via circulation through the left side of the heart to the hepatoportal circulation (>15 days) where, if it meets a partner of the opposite sex, it develops into a sexually mature adult and the pair migrate to the mesenteric veins.
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The blood supply and direction of flow in the hypophyseal portal system has been studied over many years on laboratory animals and human cadaver specimens with injection and vascular corrosion casting methods. Short portal vessels between the neural and anterior pituitary lobes provide an avenue for rapid hormonal exchange. Specifically within and between the pituitary lobes is anatomical evidence for confluent interlobe vessels, including venules providing blood from the anterior to the neural lobe, and capillary shunts exchanging blood between the intermediate and neural lobes. Such microvascular structures indicate moment-to-moment streams of information between lobes of the pituitary gland.
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As blood travels through the venules to the veins a funneling occurs called vasodilation bringing blood back to the heart. Once the blood reaches the heart it moves first into the right atrium, then the left ventricle to be pumped through the lungs for further gas exchange of carbon dioxide waste for oxygen. Oxygenated blood then flows from the lungs through the left atrium to the left ventricle where it is pumped out to the body. With respect to thermoregulation, the American flamingo has highly vascularized feet that use a countercurrent exchange system in their legs and feet.
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Diagram of the regions of the gut lymphocytes Originally it was theorized that the micro-environment of lymphoid tissues provided the cues for the preferential homing of lymphocytes. While this may be the case to some extent, it is now widely held that the main driver in lymphocyte homing is the interactions between T cell adhesion molecules (lymphocyte homing receptors) and ligands (addressins) on the tissue high endothelial venules (HEVs). This theory arose from the observation that the cell surface integrins varied between different T cell populations. Work began to identify the differences and what they meant for T cell migration.
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Since vascular beds widely express α1 receptors, the action of oxymetazoline results in vasoconstriction. In addition, the local application of the drug also results in vasoconstriction due to its action on endothelial postsynaptic α2 receptors; systemic application of α2 agonists, in contrast, causes vasodilation because of centrally-mediated inhibition of sympathetic tone via presynaptic α2 receptors. Vasoconstriction of vessels results in relief of nasal congestion in two ways: first, it increases the diameter of the airway lumen; second, it reduces fluid exudation from postcapillary venules. It can reduce nasal airway resistance (NAR) up to 35.7% and reduce nasal mucosal blood flow up to 50%.
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The dental pulp is located in the centre of a tooth, made up of living connective tissue and cells. It is surrounded by a rigid, hard and dense layer of dentine which limits the ability of the pulp to tolerate excessive build up of fluid. Normal interstitial fluid pressure in the pulp ranges from 5-20mm Hg, marked increases in pressure in the pulp due to inflammation can go up to 60mm Hg. The rise in pressure is commonly associated with an inflammatory exudate causing local collapse of the venous part of microcirculation. Tissues get starved of oxygen thus causing venules and lymphatics collapse which may lead to localized necrosis.
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The development of HEVs after prolonged inflammatory stimulus is not restricted to diseased synovium, but can also occur in other tissues, particularly the gut and thyroid. During chronic inflammation of the gut in inflammatory bowel diseases (Crohn's disease and ulcerative colitis) or the thyroid in autoimmune thyroiditis (Graves' disease and Hashimoto's thyroiditis), areas of dense lymphocytic infiltration contain vessels with plump endothelium expressing MECA-79 and HECA-452. These observations suggest that HEVs could play an important role in the pathogenesis of these diseases by mediating abnormal lymphocyte recruitment to the gut or the thyroid. MECA-79+ venules with plump endothelium have also been detected in other sites of chronic inflammation, including many cutaneous inflammatory lesions.
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The three cysteinyl leukotrienes, LTC4, LTD4, and LTE4, are potent bronchoconstrictors, increasers of vascular permeability in postcapillary venules, and stimulators of mucus secretion that are released from the lung tissue of asthmatic subjects exposed to specific allergens. They play a pathophysiological role in diverse types of immediate hypersensitivity reactions. Drugs that block their activation of the CYSLTR1 receptor viz., montelukast, zafirlukast, and pranlukast, are used clinically as maintenance treatment for allergen-induced asthma and rhinitis; nonsteroidal anti- inflammatory drug-induced asthma and rhinitis (see Aspirin-induced asthma); exercise- and cold-air induced asthma (see Exercise-induced bronchoconstriction); and childhood sleep apnea due to adenotonsillar hypertrophy (see Acquired non-inflammatory myopathy#Diet and Trauma Induced Myopathy).
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As the blood and the surrounding cells continually add and remove substances from the interstitial fluid, its composition continually changes. Water and solutes can pass between the interstitial fluid and blood via diffusion across gaps in capillary walls called intercellular clefts; thus, the blood and interstitial fluid are in dynamic equilibrium with each other. Interstitial fluid forms at the arterial (coming from the heart) end of capillaries because of the higher pressure of blood compared to veins, and most of it returns to its venous ends and venules; the rest (up to 10%) enters the lymph capillaries as lymph. Thus, lymph when formed is a watery clear liquid with the same composition as the interstitial fluid.
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Therefore, despite having clinical gingival health, a low level of inflammatory infiltrate, consisting of neutrophils, B Cell Lymphocytes and macrophages, is always present in the connective tissue underlying the junctional epithelium. Essentially, this means that histologically, there will always be an inflammatory reaction to bacteria from plaque. The constant low-level inflammatory reaction in the connective tissue underlying the junctional epithelium also results in the formation of the Gingival Crevicular Fluid (GCF). The Gingival Crevicular Fluid (GCF) is a serum like fluid that is formed from the post capillary venules of the Dentogingival Plexus which is a dense network of blood vessels within the gingival connective tissue that is sub-adjacent to the junctional epithelium.
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It is an anthelmintic with schistosomicidal activity against Schistosoma mansoni, but not against other Schistosoma spp. Oxamniquine is a potent single-dose agent for treatment of S. mansoni infection, and it causes worms to shift from the mesenteric veins to the liver, where the male worms are retained; the female worms return to the mesentery, but can no longer release eggs.Martidale, The Extra Pharmacopoeia, 31st ed, p121 Oxamniquine is a semisynthetic tetrahydroquinoline and possibly acts by DNA binding, resulting in contraction and paralysis of the worms and eventual detachment from terminal venules in the mesentry, and death. Its biochemical mechanisms are hypothesized to be related to an anticholinergic effect, which increases the parasite's motility, as well as inhibiting the synthesis of nucleic acids.
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Cilnidipine decreases blood pressure and is used to treat hypertension and its comorbidities. Due to its blocking action at the N-type and L-type calcium channel, cilnidipine dilates both arterioles and venules, reducing the pressure in the capillary bed. Cilnidipine is vasoselective and has a weak direct dromotropic effect, a strong vasodepressor effect, and an arrhythmia-inhibiting effect. Blood pressure control with cilnidipine treatment in Japanese post-stroke hypertensive patients [The CA-ATTEND study] - the results of a large-scale prospective post-marketing surveillance study of post-stroke hypertensive patients (n = 2667, male 60.4%, 69.0 ± 10.9 years) treated with cilnidipine indicate that cilnidipine was effective in treating uncontrolled blood pressure and was well tolerated in post-stroke hypertensive patients.
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With the exception of pulmonary and umbilical arteries and their corresponding veins, arteries carry oxygenated blood away from the heart and deliver it to the body via arterioles and capillaries, where the oxygen is consumed; afterwards, venules and veins carry deoxygenated blood back to the heart. Under normal conditions in adult humans at rest, hemoglobin in blood leaving the lungs is about 98–99% saturated with oxygen, achieving an oxygen delivery between 950 and 1150 ml/minEdwards Lifesciences LLC – Normal Hemodynamic Parameters – Adult 2009 to the body. In a healthy adult at rest, oxygen consumption is approximately 200–250 ml/min, and deoxygenated blood returning to the lungs is still roughly 75%Transplant Support- Lung, Heart/Lung, Heart MSN groups (70 to 78%) saturated.
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In pregnant and estrogen-treated male and female guinea pigs, clumps of Kurloff cells containing inclusion bodies of different sizes are present in large numbers in stromal tissue of the thymus and bone marrows, and the pulp cords of the spleen. In the thymus, clumps of Kurloff cells are occasionally seen at the cortico-medullary junction, scattered single cells are seen in the cortex, and numerous Kurloff cells are spotted in lymphatics and venules. In the spleen, Kurloff cells are absent in the lymphoid tissue of the white pulp, whereas there are large numbers in the red pulp. In the vertebral bone marrow, Kurloff cells are seen scattered as single cells and in clumps in random pattern among the hematopoietic cells in the stroma.
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There are CD4+ Th lymphocytes in germinal centres and interfollicular area and CD8+ T cells mainly in interfollicular area. High endothelial venules (HEVs) are also present in BALT in T/B-cell interface, allowing for the recruitment of naive T cells. These HEV are the only entry site for lymphocytes to migrate into the BALT and leave by efferent lymphatic vessels. In some species, M cells have been described in epithelium above BALT similar to M cells in the dome epithelium of Peyer’s patches, although the dome epithelium is not typical for BALT. For formation of BALT in mice is necessary inteleukin-17 and VCAM-1, PNAd and LFA-1 and it is lymphotoxin-α independent whereas the development of secondary lymphoid organs (such as lymph nodes and Peyer’s patches) is typically dependent on LTα.
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Cerebral vasculitis (sometimes the word angiitis is used instead of "vasculitis") is vasculitis (inflammation of the blood vessel wall) involving the brain and occasionally the spinal cord. It affects all of the vessels: very small blood vessels (capillaries), medium-size blood vessels (arterioles and venules), or large blood vessels (arteries and veins). If blood flow in a vessel with vasculitis is reduced or stopped, the parts of the body that receive blood from that vessel begins to die. It may produce a wide range of neurological symptoms, such as headache, skin rashes, feeling very tired, joint pains, difficulty moving or coordinating part of the body, changes in sensation, and alterations in perception, thought or behavior, as well as the phenomena of a mass lesion in the brain leading to coma and herniation.
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There are two variants of retinal vessel analysis which are based on a special fundus camera, the Retinal Vessel Analyzer which was developed by Imedos, a medical engineering company in Jena, Germany. Basically, the Retinal Vessel Analyzer measures the diameters of small arteries (arterioles) and vein (venules) in the posterior segment of the eye. In static retinal vessel analysis this is a snapshot, in dynamic vessel analysis (DVA) a 12.5 Hz optoelectric flickering light induces a stimulation of a specific segment of the retina to which the vessels react by a change in their diameter which is quantified by the device. There are different protocols for conducting this examination; a typical procedure consists of applying flicker light three times over 20 seconds each, followed by 80 seconds relaxation time.
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Starling's equation states that the rate of leakage of fluid is determined by the difference between the two forces and also by the permeability of the vessel wall to water, which determines the rate of flow for a given force imbalance. Most water leakage occurs in capillaries or post capillary venules, which have a semi-permeable membrane wall that allows water to pass more freely than protein. (The protein is said to be reflected and the efficiency of reflection is given by a reflection constant of up to 1.) If the gaps between the cells of the vessel wall open up then permeability to water is increased first, but as the gaps increase in size permeability to protein also increases with a fall in reflection coefficient. Changes in the variables in Starling's equation can contribute to the formation of edemas either by an increase in hydrostatic pressure within the blood vessel, a decrease in the oncotic pressure within the blood vessel or an increase in vessel wall permeability.
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The MECA-79 carbohydrate epitope decorates a family of HEV counter-receptors for L-selectin, both in mouse and human16. Another mAb, HECA-452, recognizing a carbohydrate epitope expressed on human HEVs but not on other vessels, has been described. Nevertheless, unlike MECA-79, this mAb is not HEV specific: HECA-452 recognizes a carbohydrate epitope related to the sialyl-Lewis x and sialyl-Lewis a oligosaccharides and, in addition to reacting with high endothelium, crossreacts with monocytic cells, dendritic cells and a subset of skin-homing memory lymphocytes. Furthermore, two other HEV markers have been described in the mouse: #the mAb MECA-325 defines an antigen that can be induced in nonlymphoid endothelial cells by interferon γ ( IFN- γ); and #the mAb MECA-367 recognizes mucosal addressin cell adhesion molecule 1 (MAdCAM-1), a counter-receptor for L-selectin and α4β7 integrin that is expressed in mucosal HEVs and in venules of intestinal lamina propria but can be induced in nonmucosal endothelial cells by tumor necrosis factor cx (TNF- α) and IL-l.
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