Metabolic products and myocardial ischemia.
Metabolic products and myocardial ischemia.
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发表时间：
1981-02
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通讯作者：
J. R. Neely;D. Feuvray
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作者：
J. R. Neely;D. Feuvray
代谢产物在缺血心肌中蓄积，继发于冠状动脉血流减少，这阻止了血管空间的充分冲洗，并减少了氧化代谢。最显著的积累产物是NADH、H+、乳酸盐、CO2、长链酰基辅酶A和长链酰基肉毒碱。这些产物干扰ATP的产生和心肌的功能。糖酵解产生的ATP被抑制积累的NADH，H+，和乳酸。线粒体和质膜的功能可能会改变辅酶A和肉毒碱的酰基酯。线粒体膜变得结构扭曲和破碎，基质中出现含脂质的无定形密度。线粒体的结构改变更频繁地发生在接受高浓度脂肪酸的心脏中，并与CoA和肉毒碱的酰基酯的高组织水平相关。从正常心脏中分离的线粒体中加入酰基肉毒碱会导致线粒体膜出现结节状嵴和碎片。
Metabolic products accumulate in ischemic myocardium secondary to reduced coronary flow, which prevents adequate washout of vascular spaces, and to reduced oxidative metabolism. The most notable products that accumulate are NADH, H+, lactate, CO2, long-chain acyl-CoA, and long-chain acyl carnitine. These products interfere with the production of ATP and the functioning of the myocardium. Glycolytic production of ATP is inhibited by accumulation of NADH, H+, and lactate. Mitochondrial and plasma membrane function may be altered by the acyl esters of CoA and carnitine. Mitochondrial membranes become structurally distorted and fragmented, and lipid-containing amorphous densities appear in the matrix. Structural alterations of mitochondria occur more frequently in hearts receiving high concentrations of fatty acids and correlate with high tissue levels of acyl esters of CoA and carnitine. Addition of acyl carnitine to mitochondria isolated from normal hearts results in nodulose-appearing cristae and fragmentation of mitochondrial membranes.