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利血平和胍乙啶对缺血大鼠心肌碳水化合物代谢的影响。

The effect of reserpine and guanethidine on carbohydrate metabolism in ischaemic rat myocardium.

作者信息

Metz V, Bernauer W

机构信息

Department of Pharmacology, University of Freiburg, Federal Republic of Germany.

出版信息

Cardiovasc Res. 1989 May;23(5):385-9. doi: 10.1093/cvr/23.5.385.

DOI:10.1093/cvr/23.5.385
PMID:2532958
Abstract

We have investigated the role of endogenous catecholamines in myocardial carbohydrate metabolism in isolated, perfused rat hearts after left coronary artery occlusion for 30 min. A significant decrease in ATP and glycogen, and an increase in glucose-6-phosphate (G-6-P) content in the ischaemic myocardium was obtained. After depletion of the cardiac noradrenaline stores by reserpine or guanethidine pretreatment the increase in the G-6-P levels was very markedly enhanced, and the myocardial glycogen content of non-ischaemic control hearts was significantly increased by reserpine. However, the amount of glycogen broken down during the ischaemia in pretreated animals was similar to that in the ischaemic myocardium from control animals, and the decrease in the myocardial ATP was not altered by reserpine or guanethidine. Thus the well known release of noradrenaline during myocardial ischaemia is not an essential prerequisite for the activation of the ischaemic breakdown of glycogen. Rather, it is of importance for later steps in anaerobic carbohydrate metabolism, probably for the activation of phosphofructokinase, as suggested by the large ischaemic accumulation of G-6-P in noradrenaline depleted hearts.

摘要

我们研究了内源性儿茶酚胺在左冠状动脉闭塞30分钟后离体灌注大鼠心脏心肌碳水化合物代谢中的作用。结果发现,缺血心肌中的三磷酸腺苷(ATP)和糖原显著减少,而葡萄糖-6-磷酸(G-6-P)含量增加。用利血平或胍乙啶预处理耗尽心脏去甲肾上腺素储备后,G-6-P水平的升高非常明显增强,利血平使非缺血对照心脏的心肌糖原含量显著增加。然而,预处理动物缺血期间分解的糖原量与对照动物缺血心肌中的糖原量相似,心肌ATP的减少并未因利血平或胍乙啶而改变。因此,心肌缺血期间众所周知的去甲肾上腺素释放并非糖原缺血性分解激活的必要前提。相反,它对无氧碳水化合物代谢的后续步骤很重要,可能对磷酸果糖激酶的激活很重要,这一点由去甲肾上腺素耗尽的心脏中G-6-P大量缺血性积累所表明。

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引用本文的文献

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Relation between energy metabolism, glycolysis, noradrenaline release and duration of ischemia.能量代谢、糖酵解、去甲肾上腺素释放与缺血持续时间之间的关系。
Mol Cell Biochem. 1996 Jul-Aug;160-161:187-94. doi: 10.1007/BF00240049.