HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) All Versions of this Article: 288/3/H1139    most recent 01139.2003v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in ISI Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via ISI Web of Science (5) Citing Articles via Google Scholar Google Scholar Articles by Martinez, R. R. Articles by Downey, H. F. Search for Related Content PubMed PubMed Citation Articles by Martinez, R. R. Articles by Downey, H. F.

Nitric oxide contributes to right coronary vasodilation during systemic hypoxia

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

Submitted 1 December 2003 ; accepted in final form 20 October 2004

As arterial partial pressure of O₂ (Pa_O2) is reduced during systemic hypoxia, right ventricular (RV) work and myocardial O₂ consumption (MO₂) increase. Mechanisms responsible for maintaining RV O₂ demand/supply balance during hypoxia have not been delineated. To address this problem, right coronary (RC) blood flow and RV O₂ extraction were measured in nine conscious, instrumented dogs exposed to normobaric hypoxia. Catheters were implanted in the right ventricle for measuring pressure, in the ascending aorta for measuring arterial pressure and for sampling arterial blood, and in an RC vein. A flow transducer was placed around the RC artery. After recovery from surgery, dogs were exposed to hypoxia in a chamber ventilated with N₂, and blood samples and hemodynamic data were collected as chamber O₂ was reduced progressively to 8%. After control measurements were made, the chamber was opened and the dog was allowed to recover. N-nitro-L-arginine (L-NNA) was then administered (35 mg/kg, via RV catheter) to inhibit nitric oxide (NO) production, and the hypoxia protocol was repeated. RC blood flow increased during hypoxia due to coronary vasodilation, because RC conductance increased from 0.65 ± 0.05 to 1.32 ± 0.12 ml·min^–1·100 g^–1. L-NNA blunted the hypoxia-induced increase in RC conductance. RV O₂ extraction remained constant at 64 ± 4% as Pa_O2 was decreased, but after L-NNA, extraction increased to 70 ± 3% during normoxia and then to 78 ± 3% during hypoxia. RV MO₂ increased during hypoxia, but after L-NNA, MO₂ was lower at any respective Pa_O2. The relationship between heart rate times RV systolic pressure (rate-pressure product) and RV MO₂ was not altered by L-NNA. To account for L-NNA-mediated decreases in RV MO₂, O₂ demand/supply variables were plotted as functions of MO₂. Slope of the conductance-MO₂ relationship was depressed by L-NNA (P = 0.03), whereas the slope of the extraction-MO₂ relationship increased (P = 0.003). In summary, increases in RV MO₂ during hypoxia are met normally by increasing RC blood flow. When NO synthesis is blocked, the large RV O₂ extraction reserve is mobilized to maintain RV O₂ demand/supply balance. We conclude that NO contributes to RC vasodilation during systemic hypoxia.

right ventricular function; right ventricular oxygen balance; myocardial oxygen consumption

This article has been cited by other articles:

				F. M. Lynch, C. Austin, A. M. Heagerty, and A. S. Izzard Adenosine and hypoxic dilation of rat coronary small arteries: roles of the ATP-sensitive potassium channel, endothelium, and nitric oxide Am J Physiol Heart Circ Physiol, March 1, 2006; 290(3): H1145 - H1150. [Abstract] [Full Text] [PDF]

				P. Zong, J. D. Tune, and H. F. Downey Mechanisms of Oxygen Demand/Supply Balance in the Right Ventricle Experimental Biology and Medicine, September 1, 2005; 230(8): 507 - 519. [Abstract] [Full Text] [PDF]