Document Detail

Myocardial impairment in chronic hypoxia is abolished by short aeration episodes: involvement of K+ATP channels.
MedLine Citation:
PMID:  15564447     Owner:  NLM     Status:  MEDLINE    
In vivo exposure to chronic hypoxia is considered to be a cause of myocardial dysfunction, thereby representing a deleterious condition, but repeated aeration episodes may exert some cardioprotection. We investigated the possible role of ATP-sensitive potassium channels in these mechanisms. First, rats (n = 8/group) were exposed for 14 days to either chronic hypoxia (CH; 10% O(2)) or chronic hypoxia with one episode/day of 1-hr normoxic aeration (CH+A), with normoxia (N) as the control. Second, isolated hearts were Langendorff perfused under hypoxia (10% O(2), 30 min) and reoxygenated (94% O(2), 30 min) with or without 3 microM glibenclamide (nonselective K(+)(ATP) channel-blocker) or 100 microM diazoxide (selective mitochondrial K(+)(ATP) channel-opener). Blood gasses, hemoglobin concentration, and plasma malondialdehyde were similar in CH and CH+A and in both different from normoxic (P < 0.01), body weight gain and plasma nitrate/nitrite were higher in CH+A than CH (P < 0.01), whereas apoptosis (number of TUNEL-positive nuclei) was less in CH+A than CH (P < 0.05). During in vitro hypoxia, the efficiency (ratio of ATP production/pressure x rate product) was the same in all groups and diazoxide had no measurable effects on myocardial performance, whereas glibenclamide increased end-diastolic pressure more in N and CH than in CH+A hearts (P < 0.05). During reoxgenation, efficiency was markedly less in CH with respect to N and CH+A (P < 0.0001), and ratex pressure product remained lower in CH than N and CH+A hearts (P < 0.001), but glibenclamide or diazoxide abolished this difference. Glibenclamide, but not diazoxide, decreased vascular resistance in N and CH (P < 0.005 and < 0.001) without changes in CH+A. We hypothesize that cardioprotection in chronically hypoxic hearts derive from cell depolarization by sarcolemmal K(+)(ATP) blockade or from preservation of oxidative phosphorylation efficiency (ATP turnover/myocardial performance) by mitochondrial K(+)(ATP) opening. Therefore K(+)(ATP) channels are involved in the deleterious effects of chronic hypoxia and in the cardioprotection elicited when chronic hypoxia is interrupted with short normoxic aeration episodes.
Giuseppina Milano; Paola Bianciardi; Antonio F Corno; Eric Raddatz; Sandrine Morel; Ludwig K von Segesser; Michele Samaja
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Publication Detail:
Type:  Comparative Study; In Vitro; Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Experimental biology and medicine (Maywood, N.J.)     Volume:  229     ISSN:  1535-3702     ISO Abbreviation:  Exp. Biol. Med. (Maywood)     Publication Date:  2004 Dec 
Date Detail:
Created Date:  2004-11-26     Completed Date:  2005-01-13     Revised Date:  2006-11-15    
Medline Journal Info:
Nlm Unique ID:  100973463     Medline TA:  Exp Biol Med (Maywood)     Country:  United States    
Other Details:
Languages:  eng     Pagination:  1196-205     Citation Subset:  IM    
Centre Hospitalier universitaire Vaudois, CH-1011, Lausanne, Switzerland.
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MeSH Terms
Anoxia / physiopathology*
Apoptosis / physiology
Chronic Disease
Glyburide / pharmacology
Heart / drug effects*,  physiopathology*
In Situ Nick-End Labeling
Myocardial Reperfusion
Myocardium / pathology*
Organ Culture Techniques
Oxidative Stress / physiology
Potassium Channel Blockers / pharmacology
Potassium Channels / drug effects,  metabolism*
Rats, Sprague-Dawley
Reg. No./Substance:
0/Potassium Channel Blockers; 0/Potassium Channels; 10238-21-8/Glyburide

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

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