Birnbaum Y, Leor J, Kloner RA
Heart Institute, Good Samaritan Hospital, and the University of Southern California, Los Angeles, California, USA.
J Thromb Thrombolysis. 1997;4(2):185-195. doi: 10.1023/a:1008866111951.
Reperfusion injury refers to cellular death or dysfunction caused by restoration of blood flow to previously alchemic tissue. This should be differentiated from the normal reparative processes that follow an ischemic insult. Four types of reperfusion injury have been described in the literature: (1) lethal reperfusion injury, (2) nonlethal reperfusion injury, (myocardial stunning), (3) reperfusion arrhythmias, and (4) vascular injury (including the "no-reflow" phenomenon). There is continued debate whether reperfusion itself is capable of killing viable myocytes, which otherwise would have survived the ischemic insult. However, there is firm evidence for the existence of myocardial stunning following various ischemic syndromes, including reperfusion therapy for acute myocardial infarction, unstable angina pectoris, vasospastic angina, effort-induced ischemia, coronary artery bypass surgery, and cardiac transplantation. Reperfusion arrhythmia is more common after short ischemic episodes than after long ischemic periods. Thus, while reperfusion arrhythmias in the setting of acute myocardial infarction are relatively rare, reperfusion arrhythmias may be an important cause of sudden death. The "no-reflow" phenomenon has been described following reperfusion in patients with acute myocardial infarction. Three major components have been proposed as mediators of reperfusion injury: (1) oxygen free radicals, (2) the complement system, and (3) neutrophils. Numerous experimental studies have shown short-term benefit by blocking various stages of the postischemic inflammatory response. Oxygen free radicals scavengers, complement inhibition, leukocyte depletion, and the use of antibodies against various adhesion molecules have shown a reduction of infarct size in many ischemic/reperfusion experimental models. However, many of these agents failed to show a benefit in the clinical setting. Moreover, the long-term benefit of such intervention is still unknown.
再灌注损伤是指因恢复先前缺血组织的血流而导致的细胞死亡或功能障碍。这应与缺血性损伤后的正常修复过程相区分。文献中描述了四种类型的再灌注损伤：（1）致死性再灌注损伤，（2）非致死性再灌注损伤（心肌顿抑），（3）再灌注心律失常，以及（4）血管损伤（包括“无复流”现象）。再灌注本身是否能够杀死原本可在缺血性损伤中存活的存活心肌细胞，仍存在持续的争论。然而，有确凿证据表明，在各种缺血综合征后存在心肌顿抑，包括急性心肌梗死的再灌注治疗、不稳定型心绞痛、血管痉挛性心绞痛、劳力性缺血、冠状动脉旁路移植术和心脏移植。再灌注心律失常在短暂缺血发作后比在长时间缺血后更常见。因此，虽然急性心肌梗死时的再灌注心律失常相对少见，但再灌注心律失常可能是猝死的一个重要原因。急性心肌梗死患者再灌注后出现了“无复流”现象。已提出三种主要成分作为再灌注损伤的介质：（1）氧自由基，（2）补体系统，以及（3）中性粒细胞。大量实验研究表明，阻断缺血后炎症反应的各个阶段可带来短期益处。氧自由基清除剂、补体抑制、白细胞耗竭以及使用针对各种黏附分子的抗体，在许多缺血/再灌注实验模型中均显示梗死面积减小。然而，这些药物中的许多在临床环境中未能显示出益处。此外，这种干预的长期益处仍然未知。
