Considerable evidence points to the leukocyte as not only the principal mediator but the sine qua non of the acute inflammatory response. In sheep, neutrophil depletion prevents the development of endothelial injury produced by endotoxemia. The generalized Shwartzman reaction can also be abolished by depletion of neutrophils, as can lung damage following an ischemia-reperfusion injury to the lower limbs in rats.
The endothelial cells are the first and probably the most important cells to be injured by this leukocyte-mediated response, which involves release of elastase and oxygen free radicals. Loss of normal endothelial function may explain many of the events recognized in septic shock and organ failure. Whereas the healthy endothelium acts as a semiper-meable membrane, the damaged endothelium allows leakage of plasma protein and its obligate fluid volume into the interstitium. Although this leakage is sustainable and even necessary at a local level for short periods, large-scale or prolonged damage leads to contraction of the intravascular space.
In response to thrombin, platelet-activating factor, brady-ldnin, hypoxia, and increased shear stress, the endothelial monolayer is capable of intrinsic modulation of vascular tone by releasing potent vasoactive substances: endothelium-derived relaxing factor (EDRF) (composed of nitric oxide derived from L-arginine), prostacyclin (PGI), and endothelin (ET). Both EDRF and PGI are vasodilators, and their release may have an important protective function by preventing vasospasm, platelet adhesion, and thrombus formation.
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