MECHANISMS OF GLYCOLYTIC INHIBITION IN ISCHEMIC RAT HEARTS
MECHANISMS OF GLYCOLYTIC INHIBITION IN ISCHEMIC RAT HEARTS
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DOI：
10.1161/01.res.37.6.742
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发表时间：
1975-01-01
影响因子：
20.1
通讯作者：
NEELY, JR
中科院分区：
文献类型：
--
作者：
ROVETTO, MJ;LAMBERTON, WF;NEELY, JR
在离体灌注大鼠心脏中研究了糖酵解抑制缺血心肌的机制。糖酵解在甘油醛-3-磷酸脱氢酶水平上受到抑制。与缺氧心脏相比，缺血性心脏中糖酵解抑制的主要因素似乎是缺血组织中乳酸和H+的组织水平较高。在缺氧和缺氧心脏中，细胞外pH值的增加比在有氧心脏中更容易抑制糖酵解。然而，维持细胞外和细胞内的pH值只会引起缺血心脏糖酵解的适度加速。在缺氧和缺血心脏中，组织乳酸的积累和糖酵解的抑制与冠状动脉血流的减少成正比。当细胞内乳酸浓度在15 ~ 20 mM之间时，糖酵解在两种条件下都受到抑制。在有氧、缺氧和缺血性心脏中，向灌注液中添加10、20或40 mM乳酸可抑制糖酵解。乳酸的作用似乎不是通过细胞内ph的改变来介导的。由此得出结论，乳酸的积累是抑制缺血心脏中糖酵解的一个主要因素。
The mechanisms of glycolytic inhibition in ischemic myocardium were investigated in the isolated, perfused rat heart. Glycolysis was inhibited at the level of glyceraldehyde-3-phosphate dehydrogenase. The major factors that accounted for the glycolytic inhibition in the ischemic heart compared with the anoxic heart appeared to be higher tissue levels of lactate and H+ in the ischemic tissue. Increased extracellular pH inhibited glycolysis in anoxic and hypoxic hearts much more readily than it did in aerobic hearts. However, maintenance of both extracellular and intracellular pH caused only a modest acceleration of glycolysis in ischemic hearts. Accumulation of tissue lactate and inhibition of glycolysis were directly proportional to the reduction in coronary bloow flow in both anoxic and ischemic hearts. At intracellular lactate concentrations between 15 and 20 mM, glycolysis was inhibited under both conditions. Addition of either 10, 20, or 40 mM lactate to the perfusate inhibited glycolysis in aerobic, anoxic, and ischemic hearts. The effect of lactate did not appear to be mediated through changes in intracellular pH. It is concluded that accumulation of lactate represents a major factor in the inhibition of glycolysis that develops in ischemic hearts.