[Damage from reperfusion: no-reflow phenomenon]

It is well known that rapid myocardial reperfusion, obtained using thrombolysis and/or PTCA, continues to be the best treatment for evolving myocardial infarction. However, a number of experimental studies have drawn attention to the fact that myocardial recovery following reperfusion may be limited by the onset of numerous deleterious biochemical events which occur during reperfusion. Studies carried out after thrombolysis have shown that the perviousness of the vessel and the existence of flow at the level of the epicardial vessels do not necessarily correspond to the recovery of tissue perfusion since a perfusion defect may persist in the presence of angiographically documented anterograde flow. This discrepancy, which occurs during reperfusion, has been attributed to marked cellular enlargement caused by ischaemia both in irreversibly damaged areas and in those which may potentially recover. In basal conditions, endothelial-neutrophil interaction is inhibited by negatively charged molecules present on endothelial cell membranes and by the production of numerous anti-inflammatory substances. During ischemia, on the other hand, anti-inflammatory and endogenous vasodilating substances are depleted in association with the appearance, on the surface of endothelial cells, of molecules favouring leukocyte adhesion. Of these the glycoprotein which has been characterized in greatest detail is the endothelial leukocyte adhesion molecule (ELAM 1) whose production and appearance on the endothelial surface is linked to cytokine-dependent endothelium activation. Ischemia may also stimulate the activation of neutrophils secreting chemiotactical and vasoconstricting factors, and cytotoxic compounds (reactive oxygen metabolites and proteolyte enzymes).(ABSTRACT TRUNCATED AT 250 WORDS)