Endogenous nitric oxide modulates myocardial oxygen consumption in canine right ventricle

Srinath Setty, Xiaoming Bian, Johnathan D. Tune, H. Fred Downey

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1 Scopus citations


The role of endogenous nitric oxide (NO) in modulating myocardial oxygen consumption (MV̇O2) is unclear, in part because of systemic and coronary hemodynamic effects of blocking NO release. This study evaluated the effect of NO on right ventricular MV̇O2 under controlled hemodynamic conditions. In 12 open-chest dogs, Nω-nitro-L-arginine methyl ester (L-NAME, 150 μg/min), a NO synthase (NOS) blocker, was infused into the right coronary artery. Heart rate and mean aortic pressure were constant. Right coronary blood flow and right ventricular MV̇O2 were measured at normal and elevated right coronary perfusion pressures (RCP) before and after L-NAME. To avoid effects of NO synthesis blockade on right coronary blood flow, which might have altered right ventricular MV̇O2, experiments, were conducted during adenosine-induced maximal coronary vasodilation. L-NAME did not affect right coronary blood flow (P = 0.51). However, L-NAME significantly increased right ventricular MV̇O2 (6% at RCP 100 mmHg, and 21% at RCP 180 mmHg). Right coronary blood flow varied with perfusion pressure (P < 0.02), and the elevation of MV̇O2 produced by L-NAME increased at higher flows (P < 0.04), consistent with the greater shear stress-mediated release of NO. These findings indicate that endogenous NO limits right ventricular MV̇O2.

Original languageEnglish
Pages (from-to)H831-H837
JournalAmerican Journal of Physiology - Heart and Circulatory Physiology
Issue number2 50-2
StatePublished - 2001


  • Maximal vasodilation
  • N-nitro-L-arginine methyl ester
  • Open-chest dogs
  • Right coronary blood flow
  • Right coronary perfusion pressure


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