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大鼠肝脏缺血再灌注后细胞质和线粒体酶的变化。

Changes in cytoplasmic and mitochondrial enzymes in rat liver after ischemia followed by reperfusion.

作者信息

Frederiks W M, Marx F

机构信息

Laboratory of Histology and Cell Biology, University of Amsterdam, The Netherlands.

出版信息

Exp Mol Pathol. 1987 Dec;47(3):291-9. doi: 10.1016/0014-4800(87)90014-1.

Abstract

The behavior of cytoplasmic and mitochondrial enzymes has been studied in rat liver at 1, 5, and 24 hr after 60 min of ischemia using histochemical methods. This period of ischemia resulted 24 h after ischemia in liver cell necrosis in about 15% of the volume of the ischemic liver lobes. As early as after 1 hr reperfusion lactate dehydrogenase (LDH, cytoplasm) activity decreased in a certain proportion of the liver parenchymal cells, whereas glutamate dehydrogenase (GDH, mitochondrial matrix) activity started to decrease after 5 hr reperfusion; the activities of mitochondrial membrane enzymes, monoamine oxidase and succinate dehydrogenase, did not decrease before 24 hr of reperfusion. It has been concluded that the early decrease in LDH activity is caused by leakage into the blood and reflects reversible damage; when this decrease is accompanied by a decrease in GDH activity irreversible liver cell damage is assumed. Diminished activity of mitochondrial membrane enzymes, due to leakage and denaturation, is observed when real necrosis can be assessed.

摘要

利用组织化学方法,研究了大鼠肝脏在缺血60分钟后1小时、5小时和24小时时细胞质和线粒体酶的行为。这段缺血期在缺血24小时后导致缺血肝叶约15%体积的肝细胞坏死。早在再灌注1小时后,一定比例的肝实质细胞中乳酸脱氢酶(LDH,细胞质)活性就有所下降,而谷氨酸脱氢酶(GDH,线粒体基质)活性在再灌注5小时后开始下降;线粒体膜酶单胺氧化酶和琥珀酸脱氢酶的活性在再灌注24小时前并未下降。得出的结论是,LDH活性的早期下降是由于漏入血液所致,反映了可逆性损伤;当这种下降伴随着GDH活性下降时,则认为肝细胞发生了不可逆损伤。当可评估真正的坏死时,会观察到由于渗漏和变性导致的线粒体膜酶活性降低。

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