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Myocardial oxygenation and high-energy phosphate levels during K_ATP channel blockade

Departments of Medicine, Radiology, Physiology and the Center for Magnetic Resonance Research, University of Minnesota Health Sciences Center, Minneapolis, Minnesota 55455

Submitted 23 February 2003 ; accepted in final form 26 May 2003

Inhibition of ATP-sensitive K⁺ (K_ATP) channel activity has previously been demonstrated to result in coronary vasoconstriction with decreased myocardial blood flow and loss of phosphocreatine (PCr). This study was performed to determine whether the high-energy phosphate abnormality during K_ATP channel blockade can be ascribed to oxygen insufficiency. Myocardial blood flow and oxygen extraction were measured in open-chest dogs during K_ATP channel blockade with intracoronary glibenclamide, whereas high-energy phosphates were examined with ³¹P magnetic resonance spectroscopy (MRS), and myocardial deoxymyoglobin (Mb-) was determined with ¹H MRS. Glibenclamide resulted in a 20 ± 8% decrease of myocardial blood flow that was associated with a loss of phosphocreatine (PCr) and accumulation of inorganic phosphate. Mb- was undetectable during basal conditions but increased to 58 ± 5% of total myoglobin during glibenclamide administration. This degree of myoglobin desaturation during glibenclamide was far greater than we previously observed during a similar reduction of blood flow produced by a coronary stenosis (22% of myoglobin deoxygenated during stenosis). The findings suggest that reduction of coronary blood flow with an arterial stenosis was associated with a decrease of myocardial energy demands and that this response to hypoperfusion was inhibited by K_ATP channel blockade.

blood flow; myoglobin; oxygen saturation

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