Nitric oxide contributes to oxygen demand-supply balance in hypoperfused right ventricle

The present study examined the role of nitric oxide (NO) in oxygen demand-supply balance in hypoperfused canine right ventricular myocardium. The right coronary artery of anesthetized, open-chest dogs was perfused at pressures of 80, 60, and 40 mm Hg, and right ventricular myocardial oxygen consumption, right coronary blood flow and other hemodynamic and cardiac function variables were measured. Right ventricular mechanical function was indexed as the product of heart rate×peak right ventricular systolic pressure×right ventricular dP/dt _max. NO synthesis blocker N ^ω-nitro- l-arginine methyl ester (l-NAME, 150 μg/min) was infused into the right coronary artery to block NO synthesis. Neither hypoperfusion nor l-NAME altered right ventricular function. Right ventricular myocardial oxygen consumption fell with coronary perfusion pressure, but less steeply after l-NAME, and at all perfusion pressures was elevated above control. The increase in myocardial oxygen consumption in the absence of NO was met by increased oxygen extraction and by non-NO dependent vasodilation, but the relationship between flow and oxygen consumption was displaced downward after l-NAME. As right coronary perfusion pressure was reduced, the relationship between right ventricular oxygen consumption and right coronary venous PO ₂ became steeper after l-NAME, and right coronary venous PO ₂ was significantly reduced. During right coronary hypoperfusion, right ventricular function is well maintained, but myocardial oxygen consumption falls, reflecting an increase in oxygen utilization efficiency. NO contributes to this adaptation to hypoperfusion by restraining myocardial oxygen consumption, and by promoting coronary vasodilation with less severe reduction in myocardial PO ₂. NO has an important role in right ventricular oxygen demand-supply balance when right coronary perfusion pressure is reduced.