Postcapillary venules

Mebius et al. (1991) reported that the morphological and functional aspects of HEV can be studied by organ culture of mouse isolated axillary, brachial, or inguinal lymph nodes. At 24 h of culture, the appearance of the node was still quite normal, whereas the HEV became flat-walled, with a 45-50% reduction in the capacity to bind lymphocytes. This decrease in function of HEV could be reduced when lymph nodes were cultured in the presence of lipopolysaccharides. The effect of lipopoly-saccharides on the function of HEV was presumably mediated by macrophages in the subcapsular sinus, because HEV in lymph nodes, which were depleted of subcapsular sinus and medullary macrophages previous to culture, could not be stimulated by addition of lipopolysaccharides to the culture. 

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The vascular endothelium plays an important role in regulation of vascular tone and permeability. Dilatation of arterioles to increase blood flow and constriction of endothelial cells of postcapillary venules causing exsudation of plasma constituents illustrates the complex nature of this cell type. Moreover, by expression of adhesion molecules and secretion of chemokines endothelial cells play an important role in the recruitment of leukocytes to the inflamed area. Endothelial cells express two basic types of adhesion molecules on their surface ... 

Inflammation. Figure 1 Sequence of events in the recruitment of leukocytes in postcapillary venules adjacent to injured tissue. At the site of lesion, diverse reactive substances stimulate the endothelium to produce inflammatory cytokines, chemoattractants and other inflammatory mediators. The cytokine-activated endothelium expresses adhesion molecules that lead to the low affinity interactions between leukocytes and endothelium, which is mediated by selectins and described as rolling. Subsequently integrins mediate the firm adhesion of leukocytes, which allows emigration of the cells from venules into the interstitial compartment. Activated mast cells, PMNs and macrophages secrete cytokines (TNFa), lipid mediators (LTB4) and other inflammatory players (histamine, NO). 

Dietary copper deficiency increases the acute inflammatory response in rats and other small laboratory animals (Schuschke et al. 1994). The release of inflammatory mediators, such as histamine and serotonin, from mast cells increases the vascular permeability of postcapillary venules and results in edema. In copper-deficient rats, release of histamine from mast cells correlates positively with frequency of the acute inflammatory response. Copper-deficient rats (0.6 mg Cu/kg DW ration for 4 weeks) have more mast cells in muscle than copper-adequate controls given diets containing 6.3 mg Cu/kg DW ration however, histamine content of mast cells is not affected (Schuschke et al. 1994). An early clinical sign of copper deficiency is a reduction in the number of circulating neutrophils the mechanism for copper-deficient neutropenia (leukopenia in which... 

Physiologically, in both normal and hypertensive individuals, blood pressure is maintained by moment-to-moment regulation of cardiac output and peripheral vascular resistance, exerted at three anatomic sites (Figure 11-1) arterioles, postcapillary venules (capacitance vessels), and heart. A fourth anatomic control site, the kidney, contributes to maintenance of blood pressure by regulating the volume of intravascular fluid. Baroreflexes, mediated by autonomic nerves, act in combination with humoral mechanisms, including the renin-angiotensin-aldosterone system, to coordinate function at these four control sites and to maintain normal blood pressure. Finally, local release of vasoactive substances from vascular endothelium may also be involved in the regulation of vascular resistance. For example, endothelin-1 (see Chapter 17) constricts and nitric oxide (see Chapter 19) dilates blood vessels. 

Besides neuropeptides, nitric oxide is an inflammatory mediator in the airways, which is also a vasodilator and a neurotransmitter. Nitric oxide is produced by the enzymatic action of nitric oxide synthetase on L-arginine. Airways contain this enzyme in three different forms, two of which termed neuronal and endothelial nitric oxide synthetase are constitutive whereas the third form called inducible nitric oxide synthetase is inducible. The inflammatory cytokines including IL-1 and TNF-a augment the expression of inducible nitric oxide synthetase in human airway epithelial cells. Nitric oxide causes bronchodilation as a result of the relaxation of bronchial smooth muscles. It has also been suggested that nitric oxide is the neurotransmitter of the inhibitory NANC bronchodilation. The detrimental effects of nitric oxide include airway inflammation and vasodilation. It causes airway edema by increasing the erudition of plasma due to increased blood flow to postcapillary venules. The increased blood flow may also contribute to an increased mucus secretion. The role of nitric oxide in inflammatory responses has not yet been established. 

Lim, L.H., Solito, E., Russo-Marie, F., Flower, R.J., and M. Perretti, 1998, Promoting detachment of neutrophils adherent to murine postcapillary venules to control inflammation effect of lipocortin 1. Proc Natl Acad Sci USA. 24 95(24) 14535-9. 

H, N. Simionescu, M. Sinuonescu, and G,R Palade, Open junction in the endotfidium of the postcapillary venules of the diaphragm- / Cell BiaL 79 27-46 (1978). 

Within the basal lamina reside the pericytes (Fig. 1). Mesenchymal in origin, pericytes form an incomplete envelopment around the endothelial cells and within the microvascular basement membrane of capillaries and postcapillary venules. Cell bodies and cytoplasmic processes of pericytes, as well as the endothelial eells, are enveloped by the same basal lamina, except for where they make direet contact with... 

Much inflammation in asthma is thought to be a consequence of the inappropriate accumulation of eosinophils and the subsequent release of their potent proinflammatory arsenal that includes such diverse elements as granule-derived basic proteins, mediators, cytokines, and chemokines (5). Interleukin (lL)-5 is cmcial to the development and release of eosinophils from the bone marrow, their enhanced adhesion to endothelial cells that line the postcapillary venules, and their persistence, activation, and secretion in the tissues. Several animal models of asthma including the use of primates have provided good evidence... 

For the second route, leukocytes reach the CNS from blood to subarachnoid space. In this pathway, leukocytes travel from the internal carotid artery, across postcapillary venules at the pial surface of the brain into the subarachnoid space and the Virchow-Robin perivascular spaces. There, they might encounter cells of the monocyte/myeloid lineage that are competent for antigen presentation. The perivascular regions, wkere there is direct communication with the CSF compartment, are considered probable sites of lymphocyte-APC interaction and therefore, of immune surveillance of CNS. This pathway is also dependent on P-selecdn. 

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