Lurie K G, Argentieri T M, Sheldon J, Frame L H, Matschinsky F M
Am J Physiol. 1987 Sep;253(3 Pt 2):H662-70. doi: 10.1152/ajpheart.1987.253.3.H662.
Subendocardial Purkinje fibers (SEPF) have been implicated in the genesis of fatal arrhythmias that occur 24-48 h after infarction but little is known about the metabolic processes involved. Quantitative microchemical and electrophysiological studies were performed on normal and infarcted hearts removed 24 h after coronary artery occlusion. ATP, ADP, AMP, total adenine nucleotide content, phosphocreatine (PCr), and inorganic phosphate in superficial subendocardial Purkinje fibers from infarct preparations decreased approximately 30% compared with normal preparations. The phosphate potential decreased 45% in the infarct group. Similar changes were observed in adjacent contractile muscle between normals and infarcts. Action potentials of SEPF from infarct hearts had increased automaticity, markedly prolonged action potential durations at 50 and 90% repolarization (APD50 or APD90), but unchanged resting membrane potentials. The decrease in ATP, total adenine nucleotides, and the phosphate potential correlated linearly with APD50 and APD90. No correlation was found between PCr and APD90. This combined biochemical and electrophysiological approach provides a promising new way to further probe the biochemical basis of the abnormal electrical properties of subendocardial Purkinje fibers after myocardial infarction.
心内膜下浦肯野纤维（SEPF）与心肌梗死后24 - 48小时发生的致命性心律失常的发生有关，但对其中涉及的代谢过程知之甚少。对冠状动脉闭塞24小时后取出的正常和梗死心脏进行了定量微化学和电生理研究。与正常标本相比，梗死标本的心内膜下浅层浦肯野纤维中的ATP、ADP、AMP、总腺嘌呤核苷酸含量、磷酸肌酸（PCr）和无机磷酸盐减少了约30%。梗死组的磷酸势能下降了45%。在正常和梗死的相邻收缩肌中也观察到了类似的变化。梗死心脏的SEPF动作电位的自律性增加，在复极化50%和90%时动作电位持续时间（APD50或APD90）明显延长，但静息膜电位不变。ATP、总腺嘌呤核苷酸和磷酸势能的降低与APD50和APD90呈线性相关。未发现PCr与APD90之间存在相关性。这种生化和电生理相结合的方法为进一步探究心肌梗死后心内膜下浦肯野纤维电特性异常的生化基础提供了一种有前景的新途径。
