Myocardial ischemia/reperfusion protection using monophosphoryl lipid a is abrogated by the ATP-sensitive potassium channel blocker, glibenclamide

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Ischemic preconditioning during coronary angioplasty is prevented by glibenclamide, a selective ATP-sensitive K+ channel blocker.

BACKGROUND Brief episodes of ischemia render the heart more resistant to subsequent ischemia; this phenomenon has been called ischemic preconditioning. In some animal species, myocardial preconditioning appears to be due to activation of ATP-sensitive K+ (KATP) channels. The role played by KATP channels in preconditioning in humans remains unknown. The aim of this study was to establish whether...

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

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The effects of ATP-dependent potassium channel opener; pinacidil, and blocker; glibenclamide, on the ischemia induced arrhythmia in partial and complete ligation of coronary artery in rats

Objective(s): Electrical inhomogeneity between ischemic and non ischemic myocardium is the basis of arrhythmia which occurs following coronary artery occlusion. The leakage of potassium from the ischemic region to the non ischemic region is very effective in the generation of these arrhythmias. The aim of this study is to research the effect of ATP-dependent potassium (KATP) channel blocker (gl...

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ATP-sensitive K1 channel blocker glibenclamide and diaphragm fatigue during normoxia and hypoxia

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ATP-sensitive K+ channel blocker glibenclamide and diaphragm fatigue during normoxia and hypoxia.

The role of ATP-sensitive K+ channels in skeletal muscle contractile performance is controversial: blockers of these channels have been found to not alter, accelerate, or attenuate fatigue. The present study reexamined whether glibenclamide affects contractile performance during repetitive contraction. Experiments systematically assessed the effects of stimulation paradigm, temperature, and pre...

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ژورنال

عنوان ژورنال: Cardiovascular Research

سال: 1996

ISSN: 0008-6363

DOI: 10.1016/s0008-6363(96)00154-x