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Articles in PresS, published online ahead of print October 15, 2001
Am J Physiol Heart Circ Physiol, 10.1152/ajpheart.00398.2001
Submitted on May 11, 2001
Accepted on October 8, 2001
1 Department of Integrative Physiology, University of North Texas Health Science Center, Fort Worth, Texas, USA
* To whom correspondence should be addressed. E-mail: ssetty{at}hsc.unt.edu.
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 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, N
-nitro-L-arginine methyl ester (L-NAME, 150 ug/min, i.c.). 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 X right ventricular dP/dtmax 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.
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