1987 Volume 51 Issue 1 Pages 107-113
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 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.
