Energy metabolism and contractile function after 15 beats of moderate myocardial ischemia.
Energy metabolism and contractile function after 15 beats of moderate myocardial ischemia.
复制标题
中度心肌缺血15次心跳后的能量代谢和收缩功能。
DOI：
10.1161/01.res.70.6.1137
复制
发表时间：
1992
影响因子：
20.1
通讯作者：
Bristow,JD
中科院分区：
文献类型：
--
作者：
Arai,AE;Pantely,GA;Thoma,WJ;Anselone,CG;Bristow,JD
在充分的时间分辨率下研究心肌代谢的困难导致了关于在缺血早期引起收缩异常的机制的相互矛盾的结论。在使用急性仪器的猪身上，我们调查了在部分心肌缺血发作后的最初几次心跳中，心内膜下ATP、磷酸肌酸或乳酸含量的异常是否发展得足够快，从而导致收缩衰竭。在冠状动脉左前降支血流减少40%-50%的前15次内，局部心肌功能显著降低，但仍在继续恶化。缺血开始后第15次心跳(+/-1.5次)的快速冰冻左室壁活检显示，心内膜下磷酸肌酸和三磷酸腺苷水平显著下降，分别为对照组的77%(p<0.005)和84%(p<0.005)，但乳酸含量变化很小。通过跨壁平均值评估的代谢效应需要更长的时间才能被检测到；因此，有一种倾向于低估心内膜下代谢效应对心肌功能的重要性。当在这一早期时间段评估左室前负荷时，左室舒张期壁厚度仅减少3%，尽管冠脉灌注压大幅下降，但左室舒张末压力并没有显著变化。因此，在一个活体猪模型中，通过优化技术来检测非常早期的中度心肌缺血期间心内膜下代谢的变化，高能磷酸化合物的异常发生得足够快，导致心肌功能障碍的发生，而与血管扩张压力相关的预负荷介导的机制不能解释在这些条件下的功能恶化。
Difficulties in studying myocardial metabolism with adequate time resolution have led to contradictory conclusions regarding the mechanisms causing contractile abnormalities during the early stages of ischemia. In acutely instrumented swine, we investigated whether abnormalities in subendocardial ATP, phosphocreatine, or lactate content develop rapidly enough during the first few heart beats after onset of partial myocardial ischemia to contribute to contractile failure. Within the first 15 beats of a 40-50% reduction in left anterior descending coronary artery blood flow, regional myocardial function was significantly reduced but continuing to deteriorate. Rapidly frozen transmural left ventricular biopsies obtained on the 15th heart beat (+/- 1.5 beats) after the onset of ischemia revealed significant decrements in subendocardial phosphocreatine and ATP levels to 77% (p less than 0.05) and 84% (p less than 0.005) of control values, respectively, but minimal change in lactate content. Metabolic effects as assessed by transmural averages took longer to become detectable; thus, there was a tendency to underestimate the importance of subendocardial metabolic effects on myocardial function. When left ventricular preload was assessed during this early time period, left ventricular end-diastolic wall thickness only decreased by 3%, and left ventricular end-diastolic pressure did not change significantly despite a large fall in coronary perfusion pressure. Thus, in an in vivo pig model with techniques optimized to detect subendocardial metabolic changes within the period of very early moderate myocardial ischemia, abnormalities in high energy phosphate compounds occurred rapidly enough to contribute to developing myocardial dysfunction, whereas preload-mediated mechanisms related to vascular distending pressure could not explain the functional deterioration under these conditions.