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.
Inspiratory muscle weakness in patients with CHF is a result of a complex interplay between decreased total number of diaphragmatic actin-myosin cross-bridges (33), reduction in type IIb fibers (34), decreased regional blood flow, activation of the ubiquitin-protea-some proteolytic pathway by TNF-[alpha], decrease in various oxidative enzymes, size and number of mitochondria (35), atrophy of the limb muscle fibers,
postcapillary pulmonary hypertension with compensatory vascular remodeling, bronchial congestion, decreased lung compliance and consequently increased work of the diaphragm up to threefold (36-37) and, to some extent, hyperpnea that could predispose to hyperinflation (38,39).
Among some of the proposed phenotypes are mixed precapillary and
postcapillary PH, severe PH in respiratory disease, HIV-associated PH, portopulmonary hypertension, connective tissue disease-associated PH, and PAH in children.
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).
A postulated mechanism for necrotizing vasculitis in hepatitis C virus infection is a deposition of circulating immune complexes in
postcapillary venules.
For excluding
postcapillary pulmonary hypertension, the PAWP was determined.
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.
vasodilator of
postcapillary venules which cause increased vascular permeability in
postcapillary venules, leading to protein extravasation (tissue edema)
Together, the arterioles, associated capillary network, and
postcapillary venules form a functional unit called the microcirculatory or microvascular bed of that tissue.
The first reports of eczematous inflammation within congenital malformations of
postcapillary venules appeared in the mid-1990s with descriptions of dermatitis within nuchal-occipital port wine stains (PWS) in children (1, 2).
The interaction between neutrophils and vascular endothelium is a key step in the inflammatory process, which usually takes place in
postcapillary venules.
Nitric oxide is an upstream signal of vascular endothelial growth factor-induced extracellularsignal-regulated kinase 1/2 activation in
postcapillary endothelium.
