Glibenclamide, a putative ATP-sensitive K+ channel blocker, inhibits coronary autoregulation in anesthetized dogs.

• DOI: 10.1161/01.res.73.4.771
• Publication Date: 2012-06-12T00:47:05Z
• Authors: T Narishige; K Egashira; Y Akatsuka; Y Katsuda; K Numaguchi; M Sakata; A Takeshita
• Keywords: Male; 03 medical and health sciences; Adenosine Triphosphate; Dogs; Potassium Channels; 0302 clinical medicine; Coronary Circulation; Glyburide; Animals; Homeostasis; Female

We tested the hypothesis that ATP-sensitive K+ channels are involved in mechanism mediating coronary autoregulation open-chest dogs. perfused left anterior descending artery with arterial blood from an extracorporeal circuit and measured steady-state flow (CBF) stepwise changes perfusion pressure (CPP) between 50 150 mm Hg during intracoronary infusion of vehicle or glibenclamide (a putative blocker channels). CBF was relatively stable over CPP 110 infusion, indicating presence at range. During (10 micrograms.min-1 x kg-1), progressively decreased reduction below Hg, whereas CPP-CBF relation above not altered by glibenclamide. The index [1-(delta F/F)/(delta P/P), where F indicates P CPP] greater than 0 range 100 less infusion. Glibenclamide did alter systemic pressure, heart rate, ventricular regional myocardial oxygen consumption associated CPP. In absence glibenclamide, reproducible repeated studies for time control. These results suggest play important role lower blood-perfused dog heart.