Marx A, Heberer M, Gale J, Landmann J
Helv Chir Acta. 1989 Dec;56(4):539-42.
Preserved organs are damaged not only by the ischemic injury due to lack of oxygen. The reperfusion injury mediated by oxygen free radicals is an important factor in the postischemic organ failure. The prevention of free radical-induced reperfusion injury with allopurinol (AP) and superoxide dismutase (SOD) is shown in a warm ischemia kidney model. Rats were treated with allopurinol (40 mg/kg i.v.) one hour, or with SOD (20,000 IU/kg i.v.) one minute before reperfusion after a period of 35 minutes of warm ischemia. Allopurinol and SOD reduced significantly the postischemic kidney failure with a less important increase of creatinine. Creatinine levels on day three in the control group: 517 +/- 87 mumol/ml, in the SOD-group: 206 +/- 105 mumol/ml, and in the AP-group: 163 +/- 81 mumol/ml (anal. of variance: p = 0.0001). AP has a wide therapeutic range. We feel, that it is important to confirm the prevention of reperfusion injury by allopurinol prophylaxis clinically.
保存的器官不仅会因缺氧导致的缺血性损伤而受损。由氧自由基介导的再灌注损伤是缺血后器官功能衰竭的一个重要因素。在热缺血肾模型中显示了用别嘌呤醇(AP)和超氧化物歧化酶(SOD)预防自由基诱导的再灌注损伤。大鼠在35分钟热缺血后再灌注前1小时用别嘌呤醇(40mg/kg静脉注射)治疗,或在再灌注前1分钟用SOD(20,000IU/kg静脉注射)治疗。别嘌呤醇和SOD显著减轻了缺血后肾衰竭,肌酐升高程度较轻。对照组第3天的肌酐水平:517±87μmol/ml,SOD组:206±105μmol/ml,AP组:163±81μmol/ml(方差分析:p = 0.0001)。别嘌呤醇有广泛的治疗范围。我们认为,临床上通过别嘌呤醇预防来证实对再灌注损伤的预防很重要。