title: Ventricular fibrillation in preconditioned pig hearts: role of K+ATP channels.
abstract: ATP-dependent potassium (K+ATP) channels play a role in the infarct size-limiting effect of preconditioning in pigs. We previously demonstrated that preconditioning shortens monophasic action potential duration (MAPD) and accelerates the time to ventricular fibrillation (VF) during a prolonged ischemia in pigs. We sought to determine whether the mechanism of the reduced time to VF in preconditioned pigs is a consequence of K+ATP, channel activation. Pigs underwent 40 min of coronary occlusion and 2 h of reperfusion. Before this, animals received either no intervention (control), 10 min of ischemia and 10 min of reperfusion (preconditioned), or an intravenous infusion of nicorandil, a K+ATP channel opener. Additional control, preconditioned, and nicorandil-treated pigs were pretreated by glibenclamide, an antagonist of K+ATP channels. Because 1) the K+ATP channel activator nicorandil did not produce shorter time to VF, 2) the K+ATP channel inhibitor glibenclamide did not block the acceleration of VF by preconditioning, and 3) there was no relationship between time to VF and infarct size or MAPD, the major conclusion is that reduced time to VF in preconditioned animals is not a consequence of K+ATP channel activation.
authors.affiliation: Hôpital Cardiovasculaire et Pneumologique Louis Pradel, Lyon, France.
authors.forename: G
authors.initials: G
authors.lastname: Rioufol
authors.forename: M
authors.initials: M
authors.lastname: Ovize
authors.forename: J
authors.initials: J
authors.lastname: Loufoua
authors.forename: C
authors.initials: C
authors.lastname: Pop
authors.forename: X
authors.initials: X
authors.lastname: André-Fouät
authors.forename: Y
authors.initials: Y
authors.lastname: Minaire
mesh_terms: D000200:Action Potentials / Q000187:drug effects / Q000502:physiology; D000818:Animals; D001786:Blood Glucose / Q000187:drug effects / Q000378:metabolism; D001794:Blood Pressure / Q000187:drug effects; D005905:Glyburide / Q000494:pharmacology*; D006321:Heart / Q000187:drug effects / Q000503:physiopathology; D006339:Heart Rate / Q000187:drug effects; D019157:Ischemic Preconditioning, Myocardial; D009203:Myocardial Infarction / Q000473:pathology / Q000503:physiopathology; D017202:Myocardial Ischemia / Q000503:physiopathology*; D015425:Myocardial Reperfusion; D009536:Niacinamide / Q000031:analogs & derivatives* / Q000494:pharmacology; D020108:Nicorandil; D026902:Potassium Channel Blockers; D015221:Potassium Channels / Q000502:physiology*; D013552:Swine; D013997:Time Factors; D014665:Vasodilator Agents / Q000494:pharmacology; D014693:Ventricular Fibrillation / Q000503:physiopathology*
chemical_list: D001786:Blood Glucose; D026902:Potassium Channel Blockers; D015221:Potassium Channels; D014665:Vasodilator Agents; D009536:Niacinamide; D020108:Nicorandil; D005905:Glyburide