抄録
An animal experimental model which simulates human effort angina, especially in terms of diastolic abnormalities, was developted using isovolumically beating perfused rat hearts. Using this model, we studied the effects of nifedipine, a Ca2+ channel blocker. on diastolic properities during pacing-induced ischemia. When the preload of the left ventricle was set at a low level, low-flow ischemia (coronary perfusion pressure of 40mmHg) plus tachycardia (480 beats/min for 4 min) did not induce an increase in left ventricular end-diastolic pressure (LVEDP). However, with a high preload, low-flow ischemia plus pacing tachycardia indused an increase in LVEDP of 8.4±5.4mmHg (p<0.01) and a prolongation of the time constant of ventricular pressure decline (6.8±4.6msec, p<0.05) immediately after pacing tachycardia. Pretreatment with nifedipine (3×10-8M) prevented the rise in LVEDP induced by pacing tachycardia. Thus, in isolated perfused hearts, diastolic abnormalities similar to those seen in angina pectoris were obtained by low-flow ischemia plus pacing tachycardia. The response to nifedipine suggested that an alteration of Ca2+ movement may play an important role in the increase in left ventricular stiffness under these conditions.
