Mechanisms of abnormal myocardial relaxation induced by ischemia: comparison of low flow ischemia and hypoxia in isolated rabbit heart.

To investigate the mechanisms of altered myocardial diastolic stiffness and relaxation induced by myocardial oxygen deficit, we compared the hemodynamic effects of low flow ischemia (myocardial infarction model) and hypoxia in which the coronary flow was not reduced (angina pectoris model) in isolated retrograde perfused rabbit hearts. A 15-min hypoxia induced a significant increase in the left ventricular end diastolic pressure (LVEDP 10 +/- 3 to 21 +/- 7 mmHg, p less than 0.05), Po (-6 +/- 6 to 12 +/- 5 mmHg, p less than 0.01) and TB (41 +/- 8 to 54 +/- 10 ms, p less than 0.05), where Po and TB are the asymptote and the time constant of the isovolumetric left ventricular pressure decline (P = Po + A e-t/TB), respectively. There was a close linear correlation between the delta Po and delta LVEDP (t = 0.98, p less than 0.01), and between delta TB and delta LVEDP (r = 0.73, p less than 0.05). Low flow ischemia increased Po (0 +/- 4 to 2 +/- 3 mmHg, p less than 0.05) and TB (43 +/- 4 to 50 +/- 11 mmHg, NS). When DPI 201-106, a cardiotonic agent, was given to the hypoxia moded by increasing the Ca++ sensitivity of contractile proteins, further increases were observed in LVEDP (to 25 +/- 8 mmHg, p less than 0.05) and Po (to 15 +/- 7 mmHg, p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)