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MINIREVIEW

Mechanisms of Oxygen Demand/Supply Balance in the Right Ventricle

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

To whom requests for reprints should be addressed at ¹ Department of Integrative Physiology, University of North Texas Health Science Center, 3500 Camp Bowie Boulevard, Fort Worth, TX 76107. E-mail: pzong{at}hsc.unt.edu

Few studies have investigated factors responsible for the O₂ demand/supply balance in the right ventricle. Resting right coronary blood flow is lower than left coronary blood flow, which is consistent with the lesser work of the right ventricle. Because right and left coronary artery perfusion pressures are identical, right coronary conductance is less than left coronary conductance, but the signal relating this conductance to the lower right ventricular O₂ demand has not been defined. At rest, the left ventricle extracts ~75% of the O₂ delivered by coronary blood flow, whereas right ventricular O₂ extraction is only ~50%. As a result, resting right coronary venous PO₂ is ~30 mm Hg, whereas left coronary venous PO₂ is ~20 mm Hg. Right coronary conductance does not sufficiently restrict flow to force the right ventricle to extract the same percentage of O₂ as the left ventricle. Endogenous nitric oxide impacts the right ventricular O₂ demand/supply balance by increasing the right coronary blood flow at rest and during acute pulmonary hypertension, systemic hypoxia, norepinephrine infusion, and coronary hypoperfusion. The substantial right ventricular O₂ extraction reserve is used preferentially during exercise-induced increases in right ventricular myocardial O₂ consumption. An augmented, sympathetic-mediated vasoconstrictor tone blunts metabolically mediated dilator mechanisms during exercise and forces the right ventricle to mobilize its O₂ extraction reserve, but this tone does not limit resting right coronary flow. During exercise, right coronary vasodilation does not occur until right coronary venous PO₂ decreases to ~20 mm Hg. The mechanism responsible for right coronary vasodilation at low PO₂ has not been delineated. In the poorly autoregulating right coronary circulation, reduced coronary pressure unloads the coronary hydraulic skeleton and reduces right ventricular systolic stiffness. Thus, normal right ventricular external work and O₂ demand/supply balance can be maintained during moderate coronary hypoperfusion.

Key Words: right ventricle • myocardial oxygen consumption • oxygen extraction reserve • coronary circulation • contractile function

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				D. J. Duncker and R. J. Bache Regulation of Coronary Blood Flow During Exercise Physiol Rev, July 1, 2008; 88(3): 1009 - 1086. [Abstract] [Full Text] [PDF]