EFFECTS OF SUBSTRATES ON TISSUE METABOLIC CHANGES IN ISOLATED RAT-HEART DURING UNDERPERFUSION AND ON RELEASE OF LACTATE-DEHYDROGENASE AND ARRHYTHMIAS DURING REPERFUSION
EFFECTS OF SUBSTRATES ON TISSUE METABOLIC CHANGES IN ISOLATED RAT-HEART DURING UNDERPERFUSION AND ON RELEASE OF LACTATE-DEHYDROGENASE AND ARRHYTHMIAS DURING REPERFUSION
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DOI：
10.1161/01.res.43.1.102
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发表时间：
1978-01-01
影响因子：
20.1
通讯作者：
OPIE, LH
中科院分区：
文献类型：
--
作者：
BRICKNELL, OL;OPIE, LH
在Langendorff灌注的大鼠心脏中，灌注压从100厘米水柱降至20厘米水柱持续30分钟，以建立一种伴有残余氧摄取的全心缺血模型。再灌注期间乳酸脱氢酶（LDH）的释放以及室性心律失常的发生是底物依赖性的。葡萄糖灌注的心脏在缺血期间糖酵解ATP产生速率最高（每分钟2.5微摩尔/克），组织环磷酸腺苷[cAMP]含量正常。在再灌注期间，LDH的释放最低，且未发生严重的室性心律失常。在丙酮酸灌注的心脏中，缺血期间糖酵解受到抑制，糖酵解ATP产生速率仅为每分钟0.5微摩尔/克，组织cAMP增加一倍；在再灌注期间，LDH释放量高出14倍，室性心律失常更为严重。葡萄糖灌注和丙酮酸灌注的心脏中ATP和磷酸肌酸的总组织含量相似。在乙酸盐灌注的心脏中，在缺血的最后5分钟几乎没有糖酵解ATP合成，且cAMP进一步增加。乙酸盐和棕榈酸盐灌注的心脏在再灌注期间LDH释放量最大，心律失常最严重，这表明起作用的是棕榈酸盐的代谢效应而非去污剂效应。脂解不是再灌注时LDH释放的主要因素。推测糖酵解ATP在维持膜完整性方面具有作用。
In Langendorff-perfused rat hearts, the perfusion pressure was reduced from 100 cm H2O to 20 cm H2O for 30 min to produce a model of global ischemia with a residual O2 uptake. Release of lactate dehydrogenase (LDH) and the occurrence of ventricular arrhythmias during reperfusion were substrate dependent. Glucose-perfused hearts had the highest rates of glycolytic ATP production (2.5 .mu.mol/g per min) during ischemia with normal contents of tissue cyclic[c]AMP. During reperfusion, the release of LDH was lowest and severe ventricular arrhythmias did not occur. In pyruvate-perfused hearts, glycolysis was inhibited during ischemia, the rate of production of glycolytic ATP was only 0.5 .mu.mol/g per min and tissue cAMP doubled; during reperfusion, LDH release was 14-fold higher and ventricular arrhythmias were more severe. Total tissue contents of ATP and phosphocreatine were similar in glucose- and in pyruvate-perfused hearts. In hearts perfused with acetate, there was virtually no glycolytic ATP synthesized during the last 5 min of ischemia and cAMP increased further. Acetate- and palmitate-perfused hearts showed greatest release of LDH and had severest arrhythmias during reperfusion, suggesting that it was the metabolic and not the detergent effects of palmitate that were operating. Lipolysis was not a major factor in the cause of reperfusion LDH release. A role of glycolytic ATP in the maintenance of membrane integrity is postulated.