[Hemodynamic effects of disopyramide on postischemic and normal myocardium]

Abstract

The acute effects of i.v. disopyramide (1.5 mg/kg) on the hemodynamics of postischemic hearts were investigated in comparison to normal ventricles. Infusion (7 min) was started in rats 20 min after 3 x 4 min of global ischemia during the period of stable postischemic dysfunction. 15 minutes after disopyramide i.v. (vs. NaCl control data) the cardiac output was reduced to 82 +/- 4% (vs. 101 +/- 5%; p less than 0.01) and dp/dtmax to 77 +/- 5% (vs. 83 +/- 3%). The maximum isovolumic pressure generating capacity as load-independent index of myocardial contractility was reduced to 89 +/- 2% (vs. 95 +/- 2%; p less than 0.05). In contrast to the results on postischemic myocardium no measureable change of the hemodynamics was detectable after the identical dose in normal animals without left ventricular dysfunction. Our results indicate an increased sensitivity of postischemic myocardium with modestly reduced contractile function to the hemodynamic effects of disopyramide, especially to the negative-inotropic effects.