Sodium nitroprusside (0.1-10 microM) induced concentration-dependent increases in coronary flow and faster early left ventricular pressure decline without compromising systolic function.
Does exogenous nitric oxide improve myocardial relaxation in isolated ejecting guinea pig hearts?
Exogenous nitric oxide exerts direct myocardial relaxant effects in the isolated ejecting heart, independent of its vasodilator activity and without compromising systolic function.
In isolated myocytes and papillary muscles, both nitric oxide, acting through guanosine 3',5'-cyclic monophosphate (cGMP), and cGMP analogues exert a novel effect on myocardial contraction, influencing mainly the onset of relaxation. We studied the effect of the exogenous nitric oxide donor, sodium nitroprusside (0.1-10 microM), in isolated ejecting guinea pig hearts at constant filling pressure, afterload, and heart rate to identify its direct myocardial effects in the whole heart. Sodium nitroprusside induced concentration-dependent increases in coronary flow as well as premature and faster early left ventricular (LV) pressure decline, but did not change end-diastolic or peak LV pressure or peak rate of rise of LV pressure. There was no correlation between changes in coronary flow and LV pressure decline. Sodium nitroprusside effects were inhibited by hemoglobin, which inactivates nitric oxide. The cGMP-independent vasodilator nicardipine also increased coronary flow but did not influence early LV pressure fall. Thus exogenous nitric oxide exerts novel direct myocardial relaxant effects in the isolated ejecting heart, independent of its known vasodilator activity, and without compromising systolic function.
Grocott-Mason et al. (Sun,) reported a other. Sodium nitroprusside vs. Nicardipine was evaluated on Coronary flow and left ventricular pressure decline. Sodium nitroprusside (0.1-10 microM) induced concentration-dependent increases in coronary flow and faster early left ventricular pressure decline without compromising systolic function.