Canadian Health&Care; Mall

Another circulatory condition resulting in impairment of endothelial-derived vasorelaxation is myocardial ischemia and reperfusion injury. An important factor response for myocardial necrosis is postischemic reperfusion injury. Classically, the explanation for this phenomenon entails the release of lipid and peptide mediators that act as chemoat-tractant and chemokinetic agents to recruit neutrophils to the site of the ischemic coronary vasculature and cause them to stick to the endothelium. We have already discussed TNF in this regard, but leukotrienes (eg, LTB4, LTC4, and LTD*) as well as thromboxanes (eg, TXAJ also contribute significantly to these events. Once neutrophils adhere to the vascular endothelium of an ischemic region, they in turn release cytotoxic mediators (eg, free radicals, leukotoxins), which are major contributors to the myocardial damage. Free radicals (eg, superoxide radicals) are known to inactivate EDRF and thus contribute to a loss of vasoactive control. However, free radicals may be produced by other cell types, including endothelial cells, presumably dysfunctional endothelial cells, which are known to occur in myocardial ischemia.