Endothelial cells are the primary physical barrier between blood and tissue in microvessels. The other capillary and post-capillary venule wall cell is the pericyte. The literature on the biology of endothelium is appreciable but less is known about pericytes. Pericytes are morphologically, biochemically, and physiologically heterogeneous. Some of pericyte functional characteristics observed in vivo and in vitro are that they: regulate endothelial proliferation and differentiation; contract in manners that either exacerbate or stem endothelial cell junctional inflammatory leakage; function as a progenitor cell; synthesize and secrete a wide variety of vasoactive autoregulating agonists; synthesize and release structural constituents of the basement membrane and extracellular matrix. Pericytes are also involved in specific microvascular diseases. This review focuses principally on nonmesangial pericytes and specific activities such as the posttranslational, short-term responses that affect microvascular perfusion and permeability, and on pericyte-endothelial cell interaction.
Ischaemia is a common clinical event leading to local and remote injury. Evidence indicates that tissue damage is largely caused by activated neutrophils which accumulate when the tissue is reperfused. If the area of ischaemic tissue is large, neutrophils also sequester in the lungs, inducing non-cardiogenic pulmonary oedema. Ischaemia reperfusion injury is initiated by production of reactive oxygen species which initially appear responsible for the generation of chemotactic activity for neutrophils. Later, once adherent to endothelium, neutrophils mediate damage by secretion of additional reactive oxygen species as well as proteolytic enzymes, in particular elastase. Therapeutic options for limiting ischaemia reperfusion injury include inhibition of oxygen radical formation, pharmacological prevention of neutrophil activation and chemotaxis, and also the use of monoclonal antibodies which prevent neutrophil-endothelial adhesion, a prerequisite for injury.
These data suggest that PMN and their products mediate most of the lung, part of the liver, and none of the local gut injury after intestinal ischemia-reperfusion.
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