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Hypoxia 2009 Speakers
Jonathan Tune
Department of Cellular and Integrative Physiology, Indiana University School of Medicine, Indianapolis Indiana
Email: jtune@iupui.edu
Talk Title: Control of coronary blood flow during hypoxia
Session: The Heart at High Altitude
Abstract: Coronary vascular resistance is regulated by a variety of factors including arterial pressure, myocardial metabolism, autonomic nervous system as well as arterial oxygen tension (hypoxia). Progressive hypoxemia results in graded coronary vasodilation that is significantly more pronounced when arterial oxygen tension falls below 40 mmHg. The mechanisms responsible for hypoxia-induced increases in coronary blood flow have been the subject of investigations for over 75 years. Microvascular studies have demonstrated that oxygen has direct effects on vascular smooth muscle likely mediated by oxygen sensors located in terminal arterioles, capillaries and/or venules (vessels < 15 mm diameter). However, in vivo experiments suggest direct microvascular effects of oxygen contribute little to coronary vasodilation. Coronary vasomotor tone during systemic hypoxia is mediated in large part by increased production of local vasoactive metabolites in proportion to reflex-mediated increases in myocardial metabolism and diminished myocardial tissue oxygenation. Production of adenosine has been shown to increase exponentially with the degree of hypoxia and blockade or degradation of adenosine markedly impairs hypoxia-induced coronary vasodilation. Other data support the role of endothelial derived relaxing factors (nitric oxide, prostaglandins, and hyperpolarizing factors) in control of coronary blood flow during hypoxia. Additional studies demonstrate that inhibition of K+ATP channels with glibenclamide significantly impairs hypoxic coronary vasodilation. Taken together, these data support the hypothesis that the coronary vascular smooth muscle response to hypoxia depends on metabolic and endothelial vasodilatory factors that are produced in proportion to the degree of hypoxemia. These local vasodilators function, at least in part, through mechanisms depending on K+ATP channels.

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