Neutrophil interactions with endothelium and platelets: possible role in the development of cardiovascular injury.

Abstract

Polymorphonuclear neutrophils (PMN) cause myocardial injury during ischaemia and reperfusion by their direct effects on the myocardium; PMN release highly cytotoxic free oxygen radicals and proteolytic enzymes and PMN aggregates are involved in capillary plugging and the no-reflow phenomenon. In addition, PMN-derived factors including free oxygen radicals, lipoxygenase products, cytokines and proteolytic enzymes have been shown to modify the function of endothelium and platelets. However, both endothelium and platelets are capable of modulating PMN activation. Endothelial cells modulate PMN function by the expression of adhesion molecules and by release of soluble factors including nitric oxide, prostacyclin, endothelins, platelet activating factor and interleukin-8. Platelets affect PMN activation by release of thromboxane A2, platelet derived growth factor, serotonin, lipoxygenase products, proteases and adenosine. Thus, in addition to their direct injurious effect on ischaemic myocardium, neutrophils are involved in the functional balance between endothelium and platelets and exert an indirect effect on the myocardium.