[Mediators of the vascular endothelium as markers of myocardial ischemia and reperfusion].

Myocardial ischaemia may occur during spasm or thrombosis of the coronary arteries. The vascular endothelium plays an essential role in the lesions observed during ischaemia and myocardial reperfusion by the intermediary of the numerous endothelium-derived vasoactive factors. These include the "endothelium-derived relaxing factors" (EDRFs) nitrous oxide, prostacyclin, which are vasodilators and platelet antiaggregants ant the "endothelium-derived contracting factors" (EDCFs), endothelin, PGH2, oxygen-free radicals which are vasoconstrictive. The endothelial cells also produce the platelet activating factor and factors essential for coagulation. The metabolism and biological properties of these different mediators are reviewed. During the phenomena of myocardial ischemia-reperfusion, endothelial regulation is activated by tissue hypoxia and reduction of coronary flow and perfusion pressure. This regulation also depends on the functional state of the arteries (macroscopically normal or pathological). These vasomotor phenomena are associated with the effects of platelet aggregation and myocardial accumulation of neutrophil polynuclear blood cells. During the second phase of reperfusion cellular lesions are produced by the generation of cytotoxic oxygen-free radicals. Assays of mediators present a clinical interest when the modalities of sampling have been fixed (systemic blood samples or during cardiac catheterisation, sites of sampling, choice of timing of sampling with respect to the biological half lives of the mediators). Determining a correlation between the in vitro biological effects on those in isolated organs and clinical data has become possible with the improvement in techniques of sampling and the increasing collaboration between biologists and clinicians.