Araki J, Takaki M, Namba T, Mori M, Suga H
Second Department of Physiology, Okayama University Medical School, Japan.
Am J Physiol. 1995 Mar;268(3 Pt 2):H1061-70. doi: 10.1152/ajpheart.1995.268.3.H1061.
We studied the mechanoenergetic effects of a short-term Ca(2+)-free, high-Ca2+ Tyrode solution coronary perfusion in eight excised, cross-circulated canine hearts. The perfusion protocol consisted of coronary perfusion with Ca(2+)-free Tyrode solution for 10 min followed by high-Ca2+ (16 mM) Tyrode solution for 5 min. This new protocol successfully induced acute contractile failure in seven hearts, without myocardial ultrastructural changes. We studied the end-systolic pressure-volume relation (slope = Emax, a contractility index) and the relation between oxygen consumption per beat (VO2) and systolic pressure-volume area (PVA) in these failing hearts. These hearts had no increase in end-diastolic pressure at a given volume, a 40% decrease in Emax and a proportional decrease in the PVA-independent VO2 for 1-4 h, but no decrease in the oxygen cost of PVA, defined as the slope of the VO2-PVA relation. The oxygen cost of Emax for Ca2+ handling, defined as the slope of the relation between PVA-independent VO2 and Emax, was unchanged in the failing hearts. We conclude that the present protocol induced left ventricular contractile failure, primarily involving the suppression of Ca2+ handling energy for excitation-contraction coupling.
我们在8个离体交叉循环犬心脏中研究了短期无钙、高钙泰罗德溶液冠状动脉灌注的机械能量效应。灌注方案包括用无钙泰罗德溶液冠状动脉灌注10分钟，随后用高钙（16 mM）泰罗德溶液灌注5分钟。这个新方案成功地在7个心脏中诱发了急性收缩功能衰竭，且无心肌超微结构改变。我们研究了这些衰竭心脏的收缩末期压力-容积关系（斜率=Emax，收缩性指数）以及每搏耗氧量（VO2）与收缩期压力-容积面积（PVA）之间的关系。这些心脏在给定容积下舒张末期压力没有增加，Emax降低了40%，与PVA无关的VO2在1-4小时内成比例降低，但PVA的氧耗成本（定义为VO2-PVA关系的斜率）没有降低。衰竭心脏中用于钙处理的Emax的氧耗成本（定义为与PVA无关的VO2和Emax之间关系的斜率）没有变化。我们得出结论，本方案诱发了左心室收缩功能衰竭，主要涉及抑制兴奋-收缩偶联中钙处理的能量。
