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Am J Physiol Heart Circ Physiol 282: H696-H703, 2002. First published October 18, 2001; doi:10.1152/ajpheart.00398.2001
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Vol. 282, Issue 2, H696-H703, February 2002

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

Srinath Setty, Johnathan D. Tune, and H. Fred Downey

Department of Integrative Physiology, University of North Texas Health Science Center at Fort Worth, Fort Worth, Texas 76107-2699

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, Nomega -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.

right coronary circulation; right ventricular oxygen utilization efficiency; open-chest dogs; Nomega -nitro-L-arginine methyl ester


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