Paller M S, Hebbel R P
Am J Physiol. 1986 Nov;251(5 Pt 2):F839-43. doi: 10.1152/ajprenal.1986.251.5.F839.
After renal ischemia, oxygen free radicals are formed and produce tissue injury, in large part, through peroxidation of polyunsaturated fatty acids. We used an in vivo method to monitor lipid peroxidation after renal ischemia, the measurement of ethane in expired gas, to determine the time course of lipid peroxidation and the effect of several agents to limit lipid peroxidation after renal ischemia. In anesthetized rats there was no significant increase in ethane production during 60 min of renal ischemia. During the first 10 min of renal reperfusion, there was a prompt increase in ethane production from 2.9 +/- 1.3 to 6.3 +/- 1.9 pmol/min (P less than 0.05). Ethane production was significantly increased during the first 50 min of reperfusion and then rapidly tapered to base-line levels. Preischemic administration of allopurinol to prevent superoxide radical generation or the superoxide radical scavenger superoxide dismutase prevented the increase in ethane production during postischemic reperfusion. These studies confirm that there is increase lipid peroxidation following renal ischemia that can be prevented by agents which limit the formation or accumulation of oxygen free radicals. This in vivo method for measuring lipid peroxidation could also be employed to study the effects of ischemia on lipid peroxidation in other organs, as well as to monitor lipid peroxidation in other forms of injury.
肾缺血后，氧自由基形成并在很大程度上通过多不饱和脂肪酸的过氧化作用产生组织损伤。我们采用一种体内方法来监测肾缺血后的脂质过氧化，即测量呼出气体中的乙烷，以确定脂质过氧化的时间进程以及几种药物对限制肾缺血后脂质过氧化的作用。在麻醉大鼠中，肾缺血60分钟期间乙烷产量无显著增加。在肾再灌注的最初10分钟内，乙烷产量迅速从2.9±1.3增至6.3±1.9 pmol/分钟（P＜0.05）。再灌注的最初50分钟内乙烷产量显著增加，然后迅速降至基线水平。缺血前给予别嘌呤醇以防止超氧阴离子自由基生成，或给予超氧阴离子自由基清除剂超氧化物歧化酶，可防止缺血后再灌注期间乙烷产量增加。这些研究证实，肾缺血后脂质过氧化增加，而限制氧自由基形成或积累的药物可预防这种增加。这种测量脂质过氧化的体内方法也可用于研究缺血对其他器官脂质过氧化的影响，以及监测其他形式损伤中的脂质过氧化。
