Takami H, Matsuda H, Kuki S, Nishimura M, Kawashima Y, Watari H, Furuya E, Tagawa K
First Department of Surgery, Osaka University Medical School, Japan.
Pflugers Arch. 1990 Apr;416(1-2):144-50. doi: 10.1007/BF00370236.
The effects of spontaneous beating after anoxia and the pumping stress induced by a left ventricular balloon on the leakage of myocardial enzymes from the isolated perfused rat heart were investigated. Beating of the heart was arrested by perfusion with high-K+ medium. When the beating was arrested during reoxygenation after anoxia, the leakage of lactate dehydrogenase (LDH) was significantly lower than during reoxygenation with spontaneous cardiac beating. After changing from K+ arrest to spontaneous beating by perfusion with low-K+ medium during reoxygenation, the leakage of LDH increased markedly. Imposition of left ventricular wall stress on the K(+)-arrested heart by repetitive passive distension during aerobic perfusion and after 20 min and 60 min of anoxia caused LDH leakages of 1.0, 4.6 and 21.0 units/g in 30 min, respectively. Under this mechanical stress, the release of LDH as a percentage of its total myocardial activity coincided well with that of cytoplasmic aspartate aminotransferase (AST), while the percentage release of mitochondrial AST was much less. These results appeared to indicate that the leakage of cytoplasmic enzymes during reoxygenation is accelerated by cardiac beating because of fragility of the cell membranes developing during the preceding anoxia.
研究了缺氧后自发搏动以及左心室球囊诱导的泵血应激对离体灌注大鼠心脏心肌酶漏出的影响。通过用高钾培养基灌注使心脏搏动停止。当缺氧后复氧期间搏动停止时，乳酸脱氢酶（LDH）的漏出明显低于复氧期间心脏自发搏动时的漏出。在复氧期间通过用低钾培养基灌注从钾离子停搏转变为自发搏动后，LDH的漏出显著增加。在有氧灌注期间以及缺氧20分钟和60分钟后，通过重复被动扩张对钾离子停搏的心脏施加左心室壁应力，在30分钟内分别导致LDH漏出量为1.0、4.6和21.0单位/克。在这种机械应力下，LDH释放量占其心肌总活性的百分比与细胞质天冬氨酸转氨酶（AST）的情况非常吻合，而线粒体AST的释放百分比则要少得多。这些结果似乎表明，复氧期间细胞质酶的漏出因心脏搏动而加速，这是由于先前缺氧期间细胞膜变得脆弱所致。
