Kilgore K S, Lucchesi B R
Department of Pharmacology, University of Michigan Medical School, Ann Arbor 48109-0626.
Clin Biochem. 1993 Oct;26(5):359-70. doi: 10.1016/0009-9120(93)90112-j.
Development of thrombolytic therapy as a treatment for myocardial infarction has focused attention on the events that occur upon reperfusion of ischemic myocardial tissue. Although it is well documented that salvage of the ischemic myocardium is dependent upon timely reperfusion, it is likely that the very events critical for survival may, in fact, lead to further tissue injury. A widely recognized source of reperfusion injury is the generation of oxygen-derived free radicals. These reactive oxygen species, which are formed within the first moments of reperfusion, are known to be cytotoxic to surrounding cells. In addition, strong support exists for the involvement of the inflammatory system in mediating tissue damage upon reperfusion. Coincident with the recruitment of neutrophils and activation of the complement system is an increase in the loss of viable cells. Although a number of mechanisms are likely to be involved in reperfusion injury, this discussion focuses on the roles that oxygen-derived free radicals and the inflammatory system play in mediating reperfusion injury.
溶栓疗法作为治疗心肌梗死的一种方法，已将人们的注意力集中在缺血心肌组织再灌注时所发生的事件上。尽管有充分的文献记载表明，缺血心肌的挽救依赖于及时的再灌注，但事实上，那些对存活至关重要的事件可能会导致进一步的组织损伤。再灌注损伤一个广为人知的来源是氧衍生自由基的产生。这些活性氧在再灌注的最初时刻形成，已知对周围细胞具有细胞毒性。此外，有充分的证据支持炎症系统参与介导再灌注时的组织损伤。与中性粒细胞的募集和补体系统的激活同时发生的是存活细胞损失的增加。尽管再灌注损伤可能涉及多种机制，但本讨论集中在氧衍生自由基和炎症系统在介导再灌注损伤中所起的作用上。
