摘要
在离体灌流的大鼠心脏上用无能量底物和含能量代谢抑制剂的缺能液灌流后,发生心肌ATP含量降低,乳酸脱氢酶(LDH)和蛋白漏出等组织损伤。恢复能量底物再灌注后,虽然心肌ATP含量明显回升,但心肌蛋白和LDH漏出进一步增加,线粒体内钙聚集,线粒体肿胀和肌原纤维挛缩。结果提示,能量反常可能是心肌缺血后再灌注损伤的发病因素之一。
Isolated rat heart was perfused with energy-free buffer, which contained metabolic inhibitorswithout energy substrate. This energy-free perfusion induced some tissue injury, such as decrease inmyocardial ATP content, leakage of myocardial lactate dehydrogenase (LDH) and proteins. Althoughmyocardial ATP content markedly recovered after reperfusion with buffer containing energy substrate,more severe damage occurred: severe leakage of myocardial LDH and proteins, calcium accumulationin myocyte mitochondria, mitochondria swelling and myofibril contracture etc. The results suggest thatthe energy paradox may be a pathogenetic factor in reperfusion injury of postischemic myocardium.
出处
《北京医科大学学报》
CSCD
1992年第5期369-370,T024,共3页
Journal of Peking University(Health Sciences)
关键词
再灌注损伤
能量代谢
心肌缺血
Ischemia-reperfusion injury
Energy metabolism
Metabolism inhibitor