Menasché P, Grousset C, Gauduel Y, Mouas C, Piwnica A
Arch Mal Coeur Vaiss. 1986 Dec;79(13):1918-23.
Oxygen free radicals play an important role in the induction of myocardial lesions by the sequence ischaemic-reperfusion. The aim of this study was to determine whether the protection afforded by a cardioplegic solution could be improved by the addition of different anti-oxygen free radical agents. Forty isolated, perfused, rat hearts' isovolumic contraction systems were divided into 5 groups of 8. In 4 groups, cardioplegia was stopped for 90 minutes in normothermia and then reperfused for 45 minutes. These hearts received a single initial injection of either standard cardioplegic solution or a solution enriched with dismutase peroxide (200,000 U/l), reduced glutathione (0.1 mM) or peroxidase (6,000 U/l). The fifth group of hearts was continually aerobically reperfused and served as a non-ischaemic control group. Based on post-ischaemic values of the pressure developed (maximal systolic-diastolic pressure), LVdP/dt, diastolic pressure and coronary flow, the best myocardial protection was observed in those hearts given cardioplegic solution enriched with peroxidase, the haemodynamic indices being comparable to those of the non-ischaemic controls. These results confirm that myocardial protection with cardioplegic solutions can be improved by the addition of anti-oxygen free radical agents, especially peroxidase which inactivates both hydrogen peroxide (precursor of the very cytotoxic hydroxyl radical) and some hydroperoxides, so interrupting the self-sustaining chain of lipidoperoxidation and limiting the damaging effects of this reaction on the cardiac cell membranes.
氧自由基在缺血-再灌注序列诱导心肌损伤中起重要作用。本研究的目的是确定通过添加不同的抗氧自由基剂是否可以改善心脏停搏液提供的保护作用。将40个离体灌注大鼠心脏的等容收缩系统分为5组,每组8个。在4组中,心脏停搏在常温下停止90分钟,然后再灌注45分钟。这些心脏接受单次初始注射标准心脏停搏液或富含超氧化物歧化酶(200,000 U/l)、还原型谷胱甘肽(0.1 mM)或过氧化物酶(6,000 U/l)的溶液。第五组心脏持续进行有氧再灌注,作为非缺血对照组。根据缺血后产生的压力(最大收缩压-舒张压)、左心室压力变化率、舒张压和冠状动脉流量的值,在给予富含过氧化物酶的心脏停搏液的心脏中观察到最佳的心肌保护作用,血流动力学指标与非缺血对照组相当。这些结果证实,通过添加抗氧自由基剂,尤其是过氧化物酶,可以改善心脏停搏液的心肌保护作用,过氧化物酶可使过氧化氢(极具细胞毒性的羟基自由基的前体)和一些氢过氧化物失活,从而中断脂质过氧化的自我维持链,并限制该反应对心肌细胞膜的损伤作用。