“…In the acute, drug-induced heart failure model, such as that caused by large doses of the P-adrenergic-blocking agent propranolol (20,136), the calcium channel blocker verapamil (12,124), or the anesthetic agent pentobarbital (31,128), milrinone (30 pg/kg prime, followed by 3 pg/kg/min infusion) caused increases in cardiac contractile force and cardiac output, decreases in right atrial pressure and total peripheral resistance, and no changes in heart rate or blood pressure (4). Since the common mechanism of the negative inotropic effect of propranolol, verapamil, and pentobarbital involves interference with Ca2+ fluxes and intracellular Ca2 + levels (19,23,43,57,58,87,88), and since amrinone and milrinone were shown to increase myocardial Ca2+ influx (44,79,84,96), it is likely that the enhanced myocardial performance is due to increased intracellular Ca2 + .…”