Hori M, Kitakaze M, Ishida Y, Inoue M
Jpn Circ J. 1987 Jan;51(1):107-13. doi: 10.1253/jcj.51.107.
The goal of this study was to investigate the mechanisms of impaired relaxation in ischemic and reperfused hearts without asynergic wall motion. To test the hypothesis that muscle elongation during ischemia does not improve the slowed relaxation, the time constant (T) of the isovolumic left ventricular pressure decay was obtained during volume loading in 14 isolated perfused canine hearts. In the nonischemic condition (coronary perfusion pressure: 107 +/- 3 mmHg), T progressively decreased as the peak left ventricular pressure was increased by volume loading. In contrast, in the ischemic condition (coronary perfusion pressure: 51 +/- 3 mmHg), T did not decrease despite an increase in peak left ventricular pressure by volume loading. These results indicate that during ischemia the impaired relaxation is not improved by an increase in preload. Moreover, reperfusion after a brief ischemia also increased T despite an increase in the contractile force, i.e., left ventricular pressure. The maximal change in the relaxation rate occurred much earlier than the maximal overshoot of the contractile force and coincided with an increase in coronary blood flow. These results indicate that prolongation of relaxation immediately after reperfusion is partly attributable to an increase in the electile force induced by the refilling of the coronary arteries. These mechanisms of impaired relaxation during ischemia and reperfusion may deteriorate ventricular filling and hence, cardiac output.
本研究的目的是探讨无运动不协调的缺血及再灌注心脏舒张功能受损的机制。为验证缺血期间心肌拉长不能改善舒张减慢这一假说，在14只离体灌注犬心的容量负荷过程中，获取左心室等容压力衰减的时间常数（T）。在非缺血状态下（冠状动脉灌注压：107±3 mmHg），随着容量负荷使左心室压力峰值升高，T逐渐降低。相反，在缺血状态下（冠状动脉灌注压：51±3 mmHg），尽管容量负荷使左心室压力峰值升高，但T并未降低。这些结果表明，缺血期间舒张功能受损不会因前负荷增加而改善。此外，短暂缺血后的再灌注尽管收缩力即左心室压力增加，但也使T升高。舒张速率的最大变化比收缩力的最大峰值早得多出现，且与冠状动脉血流量增加同时发生。这些结果表明，再灌注后立即出现的舒张延长部分归因于冠状动脉再充盈诱导的电弹力增加。缺血和再灌注期间舒张功能受损的这些机制可能会使心室充盈恶化，进而使心输出量降低。
