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ATP-Dependent K⁺ Channels Contribute to Local Metabolic Coronary Vasodilation in Experimental Diabetes

From the Department of Integrative Physiology, University of North Texas Health Science Center, Fort Worth, Texas

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 (MVO₂) 3.4-fold, myocardial O₂ delivery 3.0-fold, and heart rate 2.4-fold. Coronary venous PO₂ decreased from 19.9 ± 0.8 mmHg at rest to 14.8 ± 0.8 mmHg during exercise. Diabetes significantly reduced myocardial O₂ delivery and lowered coronary venous PO₂ 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 PO₂ versus MVO₂ relationship in nondiabetic dogs. In diabetic dogs, however, glibenclamide further reduced myocardial O₂ delivery; coronary venous PO₂ fell to 9.0 ± 1.0 mmHg during exercise, and the slope of the coronary venous PO₂ versus MVO₂ relationship steepened. These findings indicate that K_ATP channels contribute to local metabolic coronary vasodilation in alloxan-induced diabetic dogs.

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