[Influence of canrenoate potassium (aldactone pro injections) on hemodynamics and myocardial ischemia in experimental myocardial infarct].

The effects of the positive-inotropic drug Canrenoat-Kalium (CRK) on the extent and severity of myocardial ischemic injury and on hemodynamic parameters were studied in 17 dogs following coronary occlusion. Acute myocardial infarction causes depression of left-ventricular function. There eas a significant decrease in dp/dtmax, stroke volume and cardiac output; average values for mean arterial pressure were reduced, but not significantly. There was a significant increase in left-ventricular enddiastolic pressure. Heart rate was unchanged. In the healing phase of myocardial infarction a significant elevation of left-ventricular enddiastolic pressure and a significant decrease of arterial pressure persisted, but the other parameters had returned toward normal. Intravenous administration of CRK (20 mg/kg) one hour after coronary occlusion causes a significant increase in left-ventricular dp/dtmax, cardiac output and stroke volume, but no significant change in arterial pressure, heart rate and left-ventricular enddiastolic pressure. Four days after myocardial infarction administration of CRK causes also a significant incrrease in left-ventricular dp/dtmax and -n 4 out of 5 animals an increase in stroke volume. Heart rate, arterial pressure and left-ventricular enddiastolic pressure are unchanged. There is a continuous deterioration of all hemodynamic parameters in the control group 1 hour and 96 hours after experimental myocardial infarction. This spontaneous deterioration has to be taken into consideration estimating the effect of CRK in experimental conditions. 120 epicardial electrocardiographic recordings were used to assess the extent and severity of myocardial ischemic injury. The average ST-segment elevation and the number of sites with abnormal ST-segments were significantly reduced 20 min after CRK administration. The study suggests a beneficial therapeutic role for CRK treatment of left-ventricular failure in the acute and healing phase after myocardial infarction.