Document Detail

Hypoxia-induced activation of KATP channels limits energy depletion in the guinea pig heart.
MedLine Citation:
PMID:  7653639     Owner:  NLM     Status:  MEDLINE    
The functional role of ATP-dependent potassium (KATP) in hypoxic cardiac failure was investigated in isolated guinea pig hearts with glibenclamide and rimalkalim as inhibitor and activator, respectively. Monophasic action potential duration at 90% of repolarization (MAP50), left ventricular function, and cardiac energy status (31P nuclear magnetic resonance spectroscopy) were measured during normotoxic (95% O2) and hypoxic (20% O2) perfusion. In normoxic hearts, 1 microM glibenclamide did not affect MAP50, left ventricular function, and coronary flow (n = 4). In contrast, rimalkalim rapidly shortened MAP50 and left ventricular pressure (LVP) in a dose-dependent fashion (e.g., by 60.2 +/- 3.5 and 80.8 +/- 8.2%, respectively, with 0.6 microM rimalkalim). This latter effect was reversed by 1 microM (glibenclamide (n = 4). With hypoxic perfusion, a reduction in LVP was observed, along with a shortening of the action potential (MAP90; 202 +/- 13 vs. 164 +/- 9 ms) and an increase in coronary flow. Glibenclamide (1 microM) reversed the MAP90 shortening and the increase in coronary flow. In addition, glibenclamide increased LVP transiently (n = 4). When coronary flow of hypoxic hearts was kept constant, however, glibenclamide elicited a sustained positive inotropic effect (n = 7). After glibenclamide, an increase in LVP from 54 +/- 4 to 64 +/- 3 mmHg was observed, along with a reduction in the free energy change of ATP hydrolysis from -54.5 +/- 1.9 to -52.9 +/- 0.2 nJ/mol and a further increase in the coronary venous adenosine from 269 +/- 48 to 1,680 +/- 670 nmol/l.(ABSTRACT TRUNCATED AT 250 WORDS)
U K Decking; T Reffelmann; J Schrader; H Kammermeier
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Publication Detail:
Type:  Journal Article    
Journal Detail:
Title:  The American journal of physiology     Volume:  269     ISSN:  0002-9513     ISO Abbreviation:  Am. J. Physiol.     Publication Date:  1995 Aug 
Date Detail:
Created Date:  1995-09-22     Completed Date:  1995-09-22     Revised Date:  2003-11-14    
Medline Journal Info:
Nlm Unique ID:  0370511     Medline TA:  Am J Physiol     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  H734-42     Citation Subset:  IM    
Institut für Herz und Kreislaufphysiologie, Heinrich-Heine-Universität Düsseldorf, Germany.
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MeSH Terms
Adenosine Triphosphate / physiology*
Anoxia / metabolism*
Energy Metabolism*
Glyburide / pharmacology
Guinea Pigs
Myocardium / metabolism*
Potassium Channel Blockers
Potassium Channels / physiology*
Reference Values
Reg. No./Substance:
0/Potassium Channel Blockers; 0/Potassium Channels; 10238-21-8/Glyburide; 56-65-5/Adenosine Triphosphate

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