Amrinone improves postischemic myocardial metabolism in the rat heart-lung preparation.

Amrinone, a phosphodiesterase inhibitor, is a non-glycosidic noncatecholamine with both vasodilator and positive inotropic effects. We were interested in assessing the effect of amrinone on postischemic cardiac performance in the isolated heart-lung preparation. Twenty-four male Wistar-ST rats were used. They were randomly divided into three groups. Amrinone, 10 μg·ml-1 or 100 μg·ml-1 was administered 8 min after the start of perfusion except in the control group. Ten minutes after the start of perfusion, all hearts were made globally ischemic for 8 min. Subsequently, the preparations were reperfused for 10 min. At the end of the experimental period, the hearts were freeze-clamped, and then myocardial high-energy phosphates, lactate, pyruvate, and glycogen were measured. Hemodynamic parameters in all groups decreased significantly during ischemia. However, there were no significant differences among the groups. The myocardial ATP level in the 100 μg·ml-1 group was significantly higher than that in the control group. Adenosine diphosphate (ADP) and adenosine monophosphate (AMP) levels in the 100 μg·ml-1 group were significantly lower than those in the control group. Myocardial lactate, pyruvate, and glycogen levels were not significantly different among the groups. This result suggests that amrinone improves postischemic myocardial metabolism. Although we could not measure coronary flow, amrinone might increase coronary flow with direct coronary vasodilation which would have increased the myocardial ATP and energy charge levels.