Nitric oxide modulates cardiac contractility and oxygen consumption without changing contractile efficiency.

Nitric oxide (NO) affects myocardial contractility and myocardial oxygen consumption (MV˙o 2) in vitro. In α-chloralose-anesthetized dogs instrumented for the measurements of left ventricular (LV) pressure, LV volume using a conductance catheter, coronary blood flow, and coronary venous oxygen saturation (S[Formula: see text]) using a fiber-optic catheter, LV end-systolic pressure-volume relationships (ESPVR) and the relationship between MV˙o 2 and LV pressure-volume area (PVA) were analyzed before and after intravenous infusions of the NO synthase inhibitor N G-monomethyl-l-arginine acetate (l-NMMA; 5 mg/kg, 8 dogs) and the NO substrate l-arginine (600 mg/kg, 7 dogs). l-NMMA increased the slope of the ESPVR ( E max) ( P < 0.05) without changing contractile efficiency indicated by the inverse of the slope of the MV˙o 2-PVA line.l-NMMA also increased unloaded MV˙o 2, indicated by the y-axis intercept of the MV˙o 2-PVA line ( P < 0.05). In contrast,l-arginine decreased E max( P < 0.05) while decreasing MV˙o 2( P < 0.05), and without changing contractile efficiency. The basal oxygen metabolism was not affected byl-NMMA andl-arginine. These data imply that endogenous NO spares MV˙o 2 by reducing oxygen use in excitation-contraction coupling and attenuates cardiac contractility without changing contractile efficiency.