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 (MVO2) 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 MVO2 were measured before and during graded intracoronary infusions of norepinephrine in the absence and presence of a NO synthase blocker, Nω-nitro-L-arginine methyl ester (L-NAME; 150 μg/min ic). During both conditions, right coronary blood flow and right ventricular MVO2 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 MVO2 and norepinephrine dose. However, when right ventricular function was indexed by heart rate × right ventricular maximum dP/dt × 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.
|Journal||American Journal of Physiology - Heart and Circulatory Physiology|
|Issue number||2 51-2|
|State||Published - 2002|
- N-nitro-L-arginine methyl ester
- Open-chest dogs
- Right coronary circulation
- Right ventricular oxygen utilization efficiency