Document Detail

Myocardial reactive hyperemia in experimental chronic heart failure: evidence for the role of K+ adenosine triphosphate-dependent channels and cyclooxygenase activity.
MedLine Citation:
PMID:  9330129     Owner:  NLM     Status:  MEDLINE    
BACKGROUND: Several studies suggest that coronary perfusion is abnormal in heart failure. The fact that these deficits may results in an altered coronary reserve remains controversial. Therefore, coronary adaptability to short-duration ischemia and the resultant myocardial reactive hyperemia were investigated in a model of chronic heart failure. METHODS AND RESULTS: Experiments were performed in normal and failing hamster hearts (UM-X7.1, aged > 225 days). Heart rate, left ventricular developed pressure, and coronary flow were recorded continuously before and after each 30-second ischemia in isolated perfused heart preparations. Studies were conducted under control conditions and in the presence of four inhibitors of potential mediators of the reactive hyperemia response: the nitric oxide synthase inhibitor NG-nitro-L-arginine methyl ester (30 microM), the adenosine antagonist 8-(p-sulfophenyl)theophylline (50 microM), the K+ cyclic adenosine triphosphate-dependent channel antagonist glibenclamide (10 microM), and the cyclooxygenase inhibitor indomethacin (10 microM). Baseline hemodynamic parameters were all significantly impaired in failing hearts. Under control conditions, failing hearts were able to respond adequately to a 30-second ischemia: repayment-to-debt ratio averaged 1.02 +/- 0.09 as compared with 1.10 +/- 0.09 in normal hearts (P = NS). All inhibitors significantly reduced basal coronary perfusion except for indomethacin. Of the four inhibitors of potential mediators of the myocardial reactive hyperemic response, only glibenclamide and indomethacin impaired the repayment-to-debt ratio. In their presence, repayment-to-debt ratio was reduced by 40% of the baseline response (P < .01) without significant difference between normal and failing hearts. On the contrary, NG-nitro-L-arginine methyl ester and 8-(p-sulfophenyl)theophylline did not alter the repayment-to-debt ratio. CONCLUSIONS: These observations demonstrate the capacity of the failing heart to tolerate short-duration ischemia despite the presence of significant alterations in its basal coronary perfusion. In addition, results suggest that activation of K+ adenosine triphosphate-dependent channels and the presence of cyclooxygenase by-products are important determinants of coronary adaptation to short-duration ischemia in this model of chronic heart failure.
S Viau; E Fontaine; M Véronneau; G Jasmin; L Dumont
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Journal of cardiac failure     Volume:  3     ISSN:  1071-9164     ISO Abbreviation:  J. Card. Fail.     Publication Date:  1997 Sep 
Date Detail:
Created Date:  1997-11-14     Completed Date:  1997-11-14     Revised Date:  2006-11-15    
Medline Journal Info:
Nlm Unique ID:  9442138     Medline TA:  J Card Fail     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  207-15     Citation Subset:  IM    
Département de pharmacologie, Faculté de médecine, Université de Montréal, Québec, Canada.
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MeSH Terms
Cardiac Output, Low / enzymology,  metabolism*,  physiopathology
Chronic Disease
Coronary Circulation*
Disease Models, Animal
Enzyme Inhibitors / pharmacology
Glyburide / pharmacology
Hyperemia / etiology,  metabolism*,  physiopathology*
Indomethacin / pharmacology
NG-Nitroarginine Methyl Ester / pharmacology
Potassium Channels / drug effects,  metabolism*
Prostaglandin-Endoperoxide Synthases / metabolism*
Theophylline / pharmacology
Reg. No./Substance:
0/Enzyme Inhibitors; 0/Potassium Channels; 10238-21-8/Glyburide; 50903-99-6/NG-Nitroarginine Methyl Ester; 53-86-1/Indomethacin; 58-55-9/Theophylline; EC Synthases

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