Nitric oxide modulates right ventricular flow and oxygen consumption during norepinephrine infusion

This study was designed to test if nitric oxide (NO) contributes to norepinephrine-induced right coronary vasodilation and if NO blunts the norepinephrine-induced increase in myocardial oxygen consumption (MVO(2)) in the right ventricle. In five anesthetized, open-chest dogs, mean aortic pressure, heart rate, right ventricular rate of pressure development over time (dP/dt), right coronary blood flow, and right ventricular MVO(2) were measured before and during graded intracoronary infusions of norepinephrine in the absence and presence of a NO synthase blocker, N(omega)-nitro-L-arginine methyl ester (L-NAME; 150 microg/min i.c.). During both conditions, right coronary blood flow and right ventricular MVO(2) significantly increased with graded infusions of norepinephrine. L-NAME significantly blunted the coronary hyperemic response to norepinephrine, although L-NAME did not alter the relationship between right ventricular MVO(2) and norepinephrine dose. However, when right ventricular function was indexed by heart rate x right ventricular maximum dP/dt x peak right ventricular systolic pressure, L-NAME significantly increased the oxygen cost of right ventricular function. These results indicate that NO contributes to norepinephrine-induced right coronary vasodilation and improves right ventricular oxygen utilization efficiency.