Gardner T J, Stewart J R, Casale A S, Downey J M, Chambers D E
Surgery. 1983 Sep;94(3):423-7.
Experimental data suggesting that oxygen-derived free radicals may play a role in the myocardial injury associated with ischemia and reperfusion are presented. In several studies of prolonged global myocardial ischemia, the administration of free radical scavenging agents, such as superoxide dismutase, catalase, and mannitol, resulted in significantly better recovery of left ventricular function following reperfusion. In a region-at-risk model of localized myocardial ischemia, both superoxide dismutase and allopurinol significantly reduced the extent of myocardial necrosis that developed following reversible coronary arterial branch occlusion. The manner in which oxygen-derived free radicals may be harmful is examined. In particular, the possibility that these toxic species are involved in the exacerbation of the ischemic injury that develops upon reflow and reoxygenation is examined.
本文呈现了实验数据,表明氧衍生自由基可能在与缺血及再灌注相关的心肌损伤中发挥作用。在多项关于长时间全心肌缺血的研究中,给予自由基清除剂,如超氧化物歧化酶、过氧化氢酶和甘露醇,可使再灌注后左心室功能的恢复显著改善。在局部心肌缺血的危险区域模型中,超氧化物歧化酶和别嘌呤醇均显著降低了可逆性冠状动脉分支闭塞后发生的心肌坏死范围。文中探讨了氧衍生自由基可能造成损害的方式。特别是,研究了这些毒性物质是否参与了再灌注和再氧合时发生的缺血性损伤的加重过程。