Lucchesi B R
University of Michigan Medical School, Department of Pharmacology, Ann Arbor 48109-0626.
Am J Cardiol. 1990 May 22;65(19):14I-23I. doi: 10.1016/0002-9149(90)90120-p.
Reperfusion of coronary arteries to limit myocardial ischemic injury and extent of myocardial necrosis is possible by either the use of fibrinolytic therapy, coronary angioplasty or coronary artery bypass surgery. The concept that early reperfusion may salvage jeopardized myocardium is derived from basic experimental studies which purported to demonstrate that the ultimate extent of irreversible myocardial injury could be reduced by reperfusion of the ischemic myocardium within 3 hours from the onset of regional myocardial ischemia. It is firmly established that salvage of ischemic myocardium is dependent on early restoration of blood flow to the myocardium at risk. Despite dependency on reoxygenation for ultimate survival, myocardial tissue that is reperfused and reoxygenated may be subjected to additional injurious insult due to reactive metabolites of oxygen. The cytotoxic species of oxygen are referred to as "oxygen free radicals." Coincident with the influx of inflammatory cells into the reperfused region is an additional loss of otherwise viable myocardial cells. There is strong support for the concept that the polymorphonuclear leukocyte is a contributor to the phenomenon of "reperfusion" or "reoxygenation" injury in the blood perfused heart. This discussion focuses on the role of the neutrophil as a potential contributor to the extension of tissue injury and reviews those interventions, which although in the experimental stage, offer promise of becoming therapeutically important in the future and may help elucidate the mechanisms underlying the potentially deleterious role of the neutrophil in situations involving whole blood reperfusion of the ischemic myocardium.
通过使用纤维蛋白溶解疗法、冠状动脉血管成形术或冠状动脉搭桥手术，使冠状动脉再灌注以限制心肌缺血损伤和心肌坏死范围是可行的。早期再灌注可能挽救濒危心肌这一概念源于基础实验研究，这些研究据称表明，在局部心肌缺血发作后3小时内对缺血心肌进行再灌注，可减少不可逆心肌损伤的最终范围。现已明确，缺血心肌的挽救取决于尽早恢复对濒危心肌的血流供应。尽管最终存活依赖于再氧合作用，但再灌注和再氧合的心肌组织可能会因活性氧代谢产物而受到额外的损伤性刺激。氧的细胞毒性物质被称为“氧自由基”。随着炎症细胞流入再灌注区域，原本存活的心肌细胞会进一步丢失。有充分证据支持这样的观点，即多形核白细胞是血液灌注心脏中“再灌注”或“再氧合”损伤现象的一个促成因素。本讨论聚焦于中性粒细胞作为组织损伤扩展潜在促成因素的作用，并回顾了那些虽处于实验阶段，但有望在未来具有重要治疗意义且可能有助于阐明中性粒细胞在缺血心肌全血再灌注情况下潜在有害作用机制的干预措施。
