Kunz R, Schoenberg M H, Büchler M, Jost K, Beger H G
Chirurgie I, Universität Ulm.
Klin Wochenschr. 1991 Dec 15;69(21-23):1095-8. doi: 10.1007/BF01645164.
The generation of free oxygen radicals is presumed as a substantial pathogenetic principle in reperfusion injury. Although demonstrated in gut, muscle and kidneys its role in liver reperfusion injury is still under investigation. In an experimental rat model of warm liver ischemia of 60 min and 8 h reperfusion electron resonance spectroscopy assessed the increased generation of free radicals in early reperfusion period, leading to a decrease of polyunsaturated free fatty acids in liver tissue within 15 min of reperfusion. Histologically, single cell death, local and patchy necrosis of hepatic lobuli could be observed after 8 h reperfusion (n = 6). These histologic signs of liver injury could be attenuated by administration of superoxide-dismutase in combination with catalase but not by allopurinol. Best results could be obtained by deferoxamine. This indicates that increased generation of free oxygen radicals in reperfusion is not caused by the known conversion of xanthine-dehydrogenase to -oxidase but is mediated by an increased generation of hydroxyl-radicals, which can be scavenged by deferoxamine.
游离氧自由基的产生被认为是再灌注损伤中的一个重要发病机制。尽管在肠道、肌肉和肾脏中已得到证实，但其在肝脏再灌注损伤中的作用仍在研究中。在一个60分钟热肝脏缺血和8小时再灌注的实验大鼠模型中，电子顺磁共振光谱评估了再灌注早期自由基生成的增加，导致再灌注15分钟内肝脏组织中多不饱和游离脂肪酸减少。组织学上，再灌注8小时后可观察到单细胞死亡、肝小叶局部和片状坏死（n = 6）。超氧化物歧化酶联合过氧化氢酶给药可减轻这些肝损伤的组织学迹象，但别嘌呤醇则不能。去铁胺可获得最佳效果。这表明再灌注中游离氧自由基生成的增加不是由已知的黄嘌呤脱氢酶向氧化酶的转化引起的，而是由羟基自由基生成的增加介导的，去铁胺可以清除羟基自由基。
