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Nitric oxide contributes to right coronary vasodilation during systemic hypoxia
Rodolfo R Martinez1, Srinath Setty, Pu Zong
1Department of Integrative Physiology, Univ. of North Texas Health Science Center, 3500 Camp Bowie Blvd., Fort Worth, TX 76107-2699, USA.
American Journal of Physiology. Heart and Circulatory Physiology
|October 30, 2004
Summary
During systemic hypoxia, the right ventricle increases oxygen consumption. Nitric oxide (NO) aids this by dilating coronary arteries, ensuring adequate oxygen supply to the heart muscle.
Area of Science:
- Cardiovascular Physiology
- Respiratory Physiology
Background:
- Systemic hypoxia increases right ventricular (RV) work and myocardial oxygen consumption (MVO2).
- Mechanisms balancing RV oxygen (O2) demand and supply during hypoxia are not fully understood.
Purpose of the Study:
- To investigate the role of nitric oxide (NO) in regulating right coronary (RC) blood flow and RV oxygen balance during systemic hypoxia.
Main Methods:
- Measurements of RC blood flow, RV pressure, and arterial O2 levels in conscious dogs under normobaric hypoxia.
- Administration of N-omega-nitro-L-arginine (L-NNA) to inhibit NO production and repeat hypoxia protocol.
Main Results:
- Hypoxia increased RC blood flow via vasodilation, indicated by increased RC conductance.
- L-NNA blunted hypoxia-induced vasodilation and increased RV O2 extraction, but decreased RV MVO2.
- RV O2 demand/supply balance was maintained by increased RC blood flow under normal conditions, and by enhanced O2 extraction when NO synthesis was blocked.
Conclusions:
- Nitric oxide (NO) plays a significant role in mediating coronary vasodilation during systemic hypoxia.
- The RV possesses a substantial O2 extraction reserve that can be mobilized to maintain MVO2 when NO-mediated vasodilation is impaired.