A Study on the Effect of Nitric Oxide on Myocardial Oxygen Consumption and Cardiac Contractility

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We have shown that inhibition of endogenous nitric oxide (NO) augments cardiac contractility assessed by Emax, whereas others showed that spontaneous NO donors evoke a positive inotropic effect. FK409 decomposes and releases NO spontaneously when dissolved in phosphate buffer solution at 37℃. We examined the effects of FK409 and 8-bromoguanosine-cyclic-monophosphate (8-Br-cGMP) on Emax in α-chloralose-anesthetized dogs instrumented for measurements of left ventricular (LV) pressure and volume and coronary blood flow (CBF) in the left anterior descending artery (LAD). FK409, 8-Br-cGMP or papaverine was infused into the LAD, and Emax was determined by transient inferior vena cava occlusion when CBF was increased and reached its peak. Neither drug affected heart rate or LV pressure just before the measurement of Emax. FK409 increased CBF and decreased Emax in a dose-dependent manner. 8-Br-cGMP increased CBF and decreased Emax in a dose-dependent manner. Papaverine increased mean CBF but did not affect Emax. In conclusion, NO attenuates cardiac contractility in vivo, while increasing CBF. This effect seems to be mediated by cyclic-guanosine monophosphate, a second messenger of NO.