Siminiak T, Flores N A, Sheridan D J
Academic Cardiology Unit, St. Mary's Hospital Medical School, London, U.K.
Eur Heart J. 1995 Feb;16(2):160-70. doi: 10.1093/oxfordjournals.eurheartj.a060880.
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.
多形核中性粒细胞（PMN）在缺血再灌注期间通过对心肌的直接作用导致心肌损伤；PMN释放具有高度细胞毒性的游离氧自由基和蛋白水解酶，并且PMN聚集参与毛细血管阻塞和无复流现象。此外，包括游离氧自由基、脂氧合酶产物、细胞因子和蛋白水解酶在内的PMN衍生因子已被证明可改变内皮细胞和血小板的功能。然而，内皮细胞和血小板都能够调节PMN的激活。内皮细胞通过表达黏附分子以及释放包括一氧化氮、前列环素、内皮素、血小板活化因子和白细胞介素-8在内的可溶性因子来调节PMN功能。血小板通过释放血栓素A2、血小板衍生生长因子、5-羟色胺、脂氧合酶产物、蛋白酶和腺苷来影响PMN的激活。因此，除了对缺血心肌的直接损伤作用外，中性粒细胞还参与内皮细胞和血小板之间的功能平衡，并对心肌产生间接影响。
