Buser P T, Wagner S, Wu S T, Derugin N, Parmley W W, Higgins C B, Wikman-Coffelt J
Department of Radiology, University of California, San Francisco 94143.
Circulation. 1989 Dec;80(6):1837-45. doi: 10.1161/01.cir.80.6.1837.
While calcium entry blockers have a beneficial influence on the postischemic recovery of the nonhypertrophied heart, their influence on the hypertrophied heart has not been determined. The aim of this study was to assess postischemic recovery of myocardial performance and energy metabolites in rat hearts with left ventricular hypertrophy pretreated either chronically or acutely with verapamil. Left ventricular hypertrophy was induced by suprarenal constriction of the abdominal aorta. Hemodynamics and phosphorus 31 magnetic resonance spectra were monitored simultaneously in the isolated hearts during control perfusion, after 30 minutes of global ischemia, and after 30 minutes of reperfusion. All hypertrophied hearts had significantly higher rate-pressure products than normal hearts. Compared with normal hearts, oxygen consumption was significantly lower in all hypertrophied hearts, especially untreated hypertrophied hearts. Also, before ischemia all normal or hypertrophied hearts (treated or untreated) began with comparable phosphorylation potentials (i.e., the supply of energy was not significantly different). Postischemic recovery was not related to energy supply-oxygen demand before onset of ischemia. Furthermore, it was not related to energy levels or intracellular pH during ischemia. For postischemic recovery, the rate-pressure product was 40 +/- 5% in the hypertrophied heart, 83 +/- 5% in the normal, 100 +/- 3% in the hypertrophied heart chronically treated with verapamil, and 82 +/- 5% in the hypertrophied heart acutely treated with verapamil. The degree of recovery was related to coronary flow both before and after ischemia. The latter is important for flushing deleterious metabolites and ions from the interstitial space as well as for delivery of oxygen and substrate to the myocardium.
虽然钙通道阻滞剂对未发生肥厚的心脏缺血后恢复有有益影响，但其对肥厚心脏的影响尚未确定。本研究的目的是评估用维拉帕米进行慢性或急性预处理的左心室肥厚大鼠心脏缺血后心肌功能和能量代谢物的恢复情况。通过腹主动脉肾动脉以上部位缩窄诱导左心室肥厚。在离体心脏的对照灌注期间、30分钟全心缺血后以及30分钟再灌注后，同时监测血流动力学和磷31磁共振波谱。所有肥厚心脏的心率 - 血压乘积均显著高于正常心脏。与正常心脏相比，所有肥厚心脏，尤其是未经治疗的肥厚心脏，耗氧量显著降低。此外，在缺血前，所有正常或肥厚心脏（经治疗或未经治疗）的磷酸化电位开始时相当（即能量供应无显著差异）。缺血后恢复与缺血发作前的能量供应 - 氧需求无关。此外，它与缺血期间的能量水平或细胞内pH值无关。对于缺血后恢复，肥厚心脏的心率 - 血压乘积为40±5%，正常心脏为83±5%，慢性用维拉帕米治疗的肥厚心脏为100±3%，急性用维拉帕米治疗的肥厚心脏为82±5%。恢复程度与缺血前后的冠状动脉血流有关。后者对于从间质空间冲洗有害代谢物和离子以及向心肌输送氧气和底物很重要。
