Document Detail


Control of coronary blood flow during hypoxemia.
MedLine Citation:
PMID:  18269186     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Coronary vascular resistance is regulated by a variety of factors including arterial pressure, myocardial metabolism, autonomic nervous system as well as arterial O2 tension (hypoxia). Progressive hypoxemia results in graded coronary vasodilation that is significantly more pronounced when arterial O2 tension falls below 40 mmHg. Microvascular studies have demonstrated that O2 has direct effects on vascular smooth muscle likely mediated by O2 sensors located in vessels <15 microm diameter. Recent data indicates that hypoxia-induced inhibition of the pentose phosphate pathway and the subsequent decreases in NADPH and intracellular Ca2+ represent an important O2 sensing mechanism in vascular smooth muscle. However, in vivo experiments suggest direct microvascular effects of O2 contribute little to hypoxic coronary vasodilation. The vasodilation is mediated, in part, by local vasoactive metabolites produced in proportion to the degree of hypoxemia, reflex-mediated increases in myocardial metabolism and diminished myocardial tissue oxygenation. In particular, 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 investigations support the role of endothelial derived relaxing factors (nitric oxide, prostacyclin) in control of coronary blood flow during hypoxia. Additionally, reductions in PO2 hyperpolarize coronary vascular smooth muscle via K+(ATP) channels which represent important "end effectors" that significantly contribute to hypoxic coronary vasodilation. Taken together, these data indicate that the coronary vascular response to hypoxia depends on metabolic and endothelial vasodilatory factors that are produced in proportion to the degree of hypoxemia and that function through mechanisms depending on K+(ATP), channels.
Authors:
Johnathan D Tune
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Review    
Journal Detail:
Title:  Advances in experimental medicine and biology     Volume:  618     ISSN:  0065-2598     ISO Abbreviation:  Adv. Exp. Med. Biol.     Publication Date:  2007  
Date Detail:
Created Date:  2008-02-13     Completed Date:  2008-03-10     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  0121103     Medline TA:  Adv Exp Med Biol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  25-39     Citation Subset:  IM    
Affiliation:
Department of Cellular and Integrative Physiology, Indiana University School of Medicine, Indianapolis, Indiana, USA. jtune@iupui.edu
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MeSH Terms
Descriptor/Qualifier:
Adenosine / metabolism
Anoxia / metabolism,  physiopathology*
Coronary Circulation / physiology*
Humans
Nitric Oxide / metabolism
Oxygen / metabolism
Potassium Channels / metabolism
Vasodilation
Grant Support
ID/Acronym/Agency:
HL67804/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
0/Potassium Channels; 10102-43-9/Nitric Oxide; 58-61-7/Adenosine; 7782-44-7/Oxygen

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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