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Type: Journal article
Title: Effect of ATP-sensitive potassium channel inhibition on coronary metabolic vasodilation in humans
Author: Farouque, O.
Worthley, S.
Meredith, I.
Citation: Arteriosclerosis, Thrombosis and Vascular Biology, 2004; 24(5):905-910
Publisher: Lippincott Williams & Wilkins
Issue Date: 2004
ISSN: 1079-5642
Statement of
H. M. Omar Farouque, Stephen G. Worthley and Ian T. Meredith
Abstract: <h4>Objective</h4>Experimental evidence indicates that ATP-sensitive potassium (K(ATP)) channels regulate coronary blood flow (CBF). However, their contribution to human coronary metabolic vasodilation is unknown.<h4>Methods and results</h4>Seventeen patients (12 male, age 58+/-10 years) were studied. Coronary hemodynamics were assessed before and after K(ATP) channel inhibition with subselective intracoronary glibenclamide infused at 40 microg/min in an angiographically smooth coronary artery after successful percutaneous coronary intervention to another vessel. Metabolic vasodilation was induced by 2 minutes of rapid right ventricular pacing. Coronary blood velocity was measured with a Doppler guidewire and CBF calculated. The time course of hyperemia was recorded for 2 minutes after pacing, and hyperemic volume was estimated from the area under the flow-versus-time curve (AUC). Compared with vehicle infusion (0.9% saline), glibenclamide reduced resting CBF by 9% (P=0.04) and increased resting coronary vascular resistance (CVR) by 15% (P=0.03). Glibenclamide reduced pacing-induced peak CBF (50.8+/-6.8 versus 42.0+/-5.4 mL/min, P=0.001), peak CBF corrected for baseline flow (25.1+/-4.6 versus 17.6+/-3.1 mL/min, P=0.01), and increased minimum CVR (2.6+/-0.3 versus 3.1+/-0.3 mm Hg/mL per minute, P=0.002). Compared with vehicle, glibenclamide reduced total AUC at 2 minutes (3535+/-397 versus 3027+/-326 mL, P=0.001).<h4>Conclusions</h4>Vascular K(ATP) channels appear to be involved in functional coronary hyperemia after metabolic stimulation.
Keywords: blood flow
ion channels
coronary circulation
Description: © 2004 American Heart Association. All rights reserved.
DOI: 10.1161/01.ATV.0000125701.18648.48
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