venule

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venule

[′ven·yül]
(anatomy)
A small vein.
References in periodicals archive ?
HSP, also known as anaphylactoid purpura and immunoglobulin A (IgA) vasculitis, is a small-vessel leukocytoclastic vasculitis characterized by the perivascular deposition of IgAl-based immune complexes in the walls of arterioles and postcapillary venules. (1) The clinical picture of HSP is palpable purpura, abdominal pain, arthritis, and hematuria 1-2 weeks following an upper respiratory infection.
Under physiological conditions, naive (i.e., mature, non-activated) lymphocytes migrate from the peripheral blood into lymph nodes and Peyer's patches by selectively interacting with the specialized endothelium of postcapillary venules called high endothelial venules (HEVs).
Circulating naive T cells migrate to the parenchyma of draining lymph nodes through specialized postcapillary venules called high endothelial venules (HEVs) (Figure 1).
Three to five postcapillary venules per mouse were recorded (4-6 mice per group) (1 min 20 seconds each venule) and cell adhesion quantified from one minute of the recording.
Pericytes embedded within the basement membrane of capillaries and postcapillary venules play an important role in endothelial cell proliferation, migration, and stabilization [34].
Thus the T-cells and the blood vessels, mainly postcapillary venules, may be induced to proliferate.
Together, these form the perivascular/Virchow-Robin space along with pericytes embedded in the vascular basement membrane that surrounds vascular endothelial cells, which form the BBB in postcapillary venules of the brain.
Here the cell rolling and arrest occurs primarily in the postcapillary venules. Contrarily, in the lungs leukocyte extravasation occurs primarily through the capillaries and similarly in the kidneys the site of neutrophil extravasation is the glomerular capillaries and also in the liver the postcapillary venules have an inferior role in leukocyte diapedesis as it primarily happens in the liver sinusoids.
A postulated mechanism for necrotizing vasculitis in hepatitis C virus infection is a deposition of circulating immune complexes in postcapillary venules. Initial alterations in venular permeability due to the release of vasoactive amines from platelets, basophils, and mast cells facilitate the deposition of immune complexes and these may activate the complement system or may interact directly with Fc receptors on endothelial cell membranes.
It could be due to the endothelial cell edema in the endothelium of postcapillary venules which cause obstruction in the blood flow and reduction in oxygen transport (Oliveira et al., 2002).
* vasodilator of postcapillary venules which cause increased vascular permeability in postcapillary venules, leading to protein extravasation (tissue edema)