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

Nitric oxide (NO) affects myocardial contractility and myocardial oxygen consumption (MVO2) in vitro. In alpha-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 (ScvO2) using a fiber-optic catheter, LV end-systolic pressure-volume relationships (ESPVR) and the relationship between MVO2 and LV pressure-volume area (PVA) were analyzed before and after intravenous infusions of the NO synthase inhibitor NG-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 (Emax) (P < 0.05) without changing contractile efficiency indicated by the inverse of the slope of the MVO2-PVA line. L-NMMA also increased unloaded MVO2, indicated by the y-axis intercept of the MVO2-PVA line (P < 0.05). In contrast, L-arginine decreased Emax (P < 0.05) while decreasing MVO2 (P < 0.05), and without changing contractile efficiency. The basal oxygen metabolism was not affected by L-NMMA and L-arginine. These data imply that endogenous NO spares MVO2 by reducing oxygen use in excitation-contraction coupling and attenuates cardiac contractility without changing contractile efficiency.