Document Detail

ATP-dependent K(+) channels contribute to local metabolic coronary vasodilation in experimental diabetes.
MedLine Citation:
PMID:  11916945     Owner:  NLM     Status:  MEDLINE    
This study tested whether ATP-dependent K(+) channels (K(ATP) channels) are an important mechanism of functional coronary hyperemia in conscious, instrument-implanted diabetic dogs. Data were collected at rest and during exercise before and after induction of diabetes with alloxan monohydrate (40-60 mg/kg intravenously). K(ATP) channels were inhibited with glibenclamide (1 mg/kg intravenously). In nondiabetic dogs, arterial plasma glucose concentration increased from 4.8 +/- 0.3 to 21.5 +/- 2.2 mmol/l 1 week after alloxan injection. In nondiabetic dogs, exercise increased myocardial oxygen consumption (MVO(2)) 3.4-fold, myocardial O(2) delivery 3.0-fold, and heart rate 2.4-fold. Coronary venous PO(2) decreased from 19.9 +/- 0.8 mmHg at rest to 14.8 +/- 0.8 mmHg during exercise. Diabetes significantly reduced myocardial O(2) delivery and lowered coronary venous PO(2) from 16.3 +/- 0.6 mmHg at rest to 13.1 +/- 0.9 mmHg during exercise. Glibenclamide did not alter the slope of the coronary venous PO(2) versus MVO(2) relationship in nondiabetic dogs. In diabetic dogs, however, glibenclamide further reduced myocardial O(2) delivery; coronary venous PO(2) fell to 9.0 +/- 1.0 mmHg during exercise, and the slope of the coronary venous PO(2) versus MVO(2) relationship steepened. These findings indicate that K(ATP) channels contribute to local metabolic coronary vasodilation in alloxan-induced diabetic dogs.
Johnathan D Tune; Clement Yeh; Srinath Setty; H Fred Downey
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Diabetes     Volume:  51     ISSN:  0012-1797     ISO Abbreviation:  Diabetes     Publication Date:  2002 Apr 
Date Detail:
Created Date:  2002-03-27     Completed Date:  2002-05-10     Revised Date:  2006-11-15    
Medline Journal Info:
Nlm Unique ID:  0372763     Medline TA:  Diabetes     Country:  United States    
Other Details:
Languages:  eng     Pagination:  1201-7     Citation Subset:  AIM; IM    
Department of Integrative Physiology, University of North Texas Health Science Center, Fort Worth, Texas 76107, USA.
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MeSH Terms
Blood Glucose / drug effects,  metabolism
Coronary Vessels / drug effects,  physiopathology*
Diabetes Mellitus, Experimental / physiopathology*
Glyburide / pharmacology
Heart Rate / drug effects
Hydrogen-Ion Concentration
Hypoglycemic Agents / pharmacology
Membrane Proteins / physiology*
Oxygen / blood
Oxygen Consumption / drug effects
Partial Pressure
Potassium Channels
Vasodilation / physiology*
Reg. No./Substance:
0/Blood Glucose; 0/Hypoglycemic Agents; 0/Membrane Proteins; 0/Potassium Channels; 0/mitochondrial K(ATP) channel; 10238-21-8/Glyburide; 7782-44-7/Oxygen

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