| Abstract: | This study was based on the concept that intracellular accumulation of calcium plays a role in mediating ischemic myocardial injury and that inhibition of entry of calcium into cells may have a salutary effect on the ischemic heart. Nifedipine, a potent vasodilator and inhibitor of transmembrane calcium flux, was infused into the aortic root of 6 dogs (5 microgram/kg/hr) during 2 hours of myocardial ischemia while on cardiopulmonary bypass. Seven control animals received normal saline at the same flow rate and temperature (20 degrees C). The results showed that none of the 7 control animals were able to maintain adequate aortic pressure or cardiac output after 30 to 60 minutes of normothermic reperfusion. All had marked left ventricular failure and were unresponsive to large doses of inotropic agents. In contrast, the 6 dogs treated with nifedipine were weaned from bypass either without difficulty or requiring small doses of calcium chloride and norepinephrine. Light microscopy demonstrated more marked ischemic damage in the control group than in the group of drug-treated dogs. We conclude that the concept of inhibition of transmembrane calcium flux offers a new and potent method for myocardial preservation during ischemia. |
