[The effect of K(ATP)-channel activation on the electrical stability of myocardium in rats with postinfarction cardiosclerosis].
Opening of the ATP-dependent K-channels (K(ATP) channels) upon intravenous administration of the cardioselective activator BMS 180448 (3 mg/kg) decreased the ventricular fibrillation threshold (VFT) in rats with postinfarction cardiosclerosis (PIC). Preliminary injection of the selective K(ATP) channel blocker glibenclamide (0.3 mg/kg, i.v.) completely abolished the profibrillatory effect of BMS 180448. At the same time, the mitochondrial K(ATP) channel blocker 5-hydroxydecanoic acid (5 mg/kg) did not influence the proarrhythmogen activity of BMS 180448. Simultaneous administration of the sarcoK(ATP) channel inhibitor HMR 1098 (3 mg/kg) and BMS 180448 increased the VFT up to a level in intact animals. Administration of the mitoK(ATP) channel activator diazoxide (5 mg/kg) after preliminary treatment with guanethidine (50 mg/kg) increased the VFT in rats with PIC. It is concluded that opening of the mitoK(ATP) channels increases the cardiac electrical stability in rats with PIC.
Solenkova
N V
NV
Maslov
L N
LN
Serebrov
V Iu
VIu
Lishmanov
A Iu
AIu
Bogomaz
S A
SA
Gross
G J
GJ
Grover
G J
GJ
D000255:Adenosine Triphosphate / Q000502:physiology*; D000818:Animals; D004558:Electric Stimulation; D006321:Heart / Q000503:physiopathology*; D009203:Myocardial Infarction / Q000150:complications* / Q000473:pathology; D009206:Myocardium / Q000473:pathology*; D026902:Potassium Channel Blockers / Q000494:pharmacology; D015221:Potassium Channels / Q000187:drug effects* / Q000502:physiology; D051381:Rats; D017208:Rats, Wistar; D012598:Sclerosis / Q000209:etiology; D014693:Ventricular Fibrillation / Q000209:etiology / Q000503:physiopathology*
D026902:Potassium Channel Blockers; D015221:Potassium Channels; D000255:Adenosine Triphosphate