Differential effects of diltiazem and nitroprusside on left ventricular function in experimental chronic volume overload.

To compare the hemodynamic effects of a calcium-channel blocker with those of a conventional vasodilator in the awake preinstrumented dog, diltiazem and nitroprusside were administered in equihypotensive infusions before (decrease in mean aortic pressure by 10%; p less than .001, n = 6) and after (decrease in mean aortic pressure by 12%; p less than .001) chronic volume overload (CVO) produced by an infrarenal aortocaval fistula. Diltiazem had no effect on preload either before or after CVO. The maximal rate of change in left ventricular pressure (dP/dtmax) was unaffected by diltiazem before the aortocaval fistula (decrease in dP/dtmax by 6%; p = NS) but was significantly reduced by calcium-channel blockade after CVO (decrease in dP/dtmax by 22%; p less than .001). By contrast, at matched aortic pressures nitroprusside significantly reduced left ventricular end-diastolic dimension (LVEDD) and pressure (LVEDP) in the same animals before (decrease in LVEDD by 10%, p less than .05; decrease in LVEDP by 7 +/- 2 mm Hg, p less than .001) and after CVO (decrease in LVEDD by 7%, p less than .05; decrease in LVEDP by 5 +/- 2 mm Hg, p less than .001) without altering dP/dtmax. We conclude that the calcium entry blocker diltiazem, unlike conventional vasodilators, may depress left ventricular function in CVO by direct negative inotropic properties in amounts that are without myocardial depressant effects in the presence of normal left ventricular performance.