Acyl-CoA inhibition of adenine nucleotide translocation in ischemic myocardium.
Acyl-CoA inhibition of adenine nucleotide translocation in ischemic myocardium.
复制标题
酰基辅酶A抑制缺血心肌中的腺嘌呤核苷酸易位。
作者：
A. Shug;E. Shrago;N. Bittar;J. Folts;J. Koke
本文研究了犬实验性心肌缺血后腺嘌呤核苷酸跨内线粒体膜的移位和长链酰基-辅酶A酯的组织浓度。冠脉前动脉结扎可导致腺嘌呤核苷酸转移酶活性早期下降。心脏组织中长链酰基-辅酶A酯的浓度也呈递增趋势。邻近的非缺血组织表现出介于缺血和正常心脏组织之间的变化。据推测，心肌缺血后脂肪酸氧化的减少将导致长链酰基-辅酶A酯的积累，这反过来将抑制腺嘌呤核苷酸转位。最终的结果将是降低细胞的能量电荷，对肌肉收缩和电传导产生不利影响。
The translocation of adenine nucleotides across the inner mitochondrial membrane and the tissue concentration of long-chain acyl-CoA esters were studied in dog heart after experimental myocardial ischemia. Ligation of the anterior coronary artery initiated events leading to an early decrease in adenine nucleotide translocase activity. A reciprocal increase in the concentration of heart tissue long-chain acyl-CoA esters was also observed. Adjacent nonischemic tissue showed changes intermediate between that of ischemic and normal heart tissue. It is postulated that a decrease in fatty acid oxidation after myocardial ischemia would lead to an accumulation of long-chain acyl-CoA esters, which in turn would inhibit adenine nucleotide translocation. The net result would be a lowering of the energy charge of the cell, adversely affecting muscle contraction and electrical conduction.