Bailey I A, Seymour A M, Radda G K
Biochim Biophys Acta. 1981 Aug 12;637(1):1-7. doi: 10.1016/0005-2728(81)90203-6.
(1) The recovery of perfused rat hearts experiencing various lengths of total global ischaemia was studied using 31P-NMR. Mechanical function was monitored by measuring left ventricular pressure. (2) Hearts exposed to a maximum of 14 min total global ischaemia regained stable contractile function on reperfusion. The concentration of phosphocreatine in these hearts rapidly exceeded its pre-ischaemic value while that of ATP rose very slowly. Pi fell on reflow to approximately its original level. These observations are interpreted as being the result of a rapid turnover of ATP stimulating phosphocreatine production by the mitochondrial isozyme of creatine kinase (ATP: creatine N-phosphotransferase, EC 2.7.3.2). (3) The recovery of intracellular pH on reperfusion does not depend upon the duration of ischaemia, nor on the pH or the percentage of ATP depletion at the end of the ischaemic period. This indicates that pH recovery is a flow-dependent phenomenon. (4) In non-recovering hearts, multiple Pi resonances are observed which arise from areas of differing myocardial pH. Phosphocreatine levels did not rise above 50% of their pre-ischaemic values. ATP levels remained depressed. This suggests that localized tissue necrosis only characterizes the failing situation.
(1) 使用31P-NMR研究了经历不同时长全心缺血的灌注大鼠心脏的恢复情况。通过测量左心室压力监测机械功能。(2) 暴露于最长14分钟全心缺血的心脏在再灌注时恢复了稳定的收缩功能。这些心脏中磷酸肌酸的浓度迅速超过其缺血前的值，而ATP的浓度上升非常缓慢。再灌注时无机磷酸下降至大约其原始水平。这些观察结果被解释为ATP快速周转刺激肌酸激酶线粒体同工酶（ATP：肌酸N-磷酸转移酶，EC 2.7.3.2）产生磷酸肌酸的结果。(3) 再灌注时细胞内pH的恢复不取决于缺血的持续时间，也不取决于缺血期末的pH或ATP消耗的百分比。这表明pH恢复是一种流量依赖性现象。(4) 在未恢复的心脏中，观察到多个源于不同心肌pH区域的无机磷酸共振。磷酸肌酸水平未升至其缺血前值的50%以上。ATP水平仍然很低。这表明局部组织坏死仅为衰竭情况的特征。
