Faculty Collaboration Database

[The effect of K(ATP)-channel activation on the electrical stability of myocardium in rats with postinfarction cardiosclerosis]. Eksp Klin Farmakol 2004;67(3):10-3

Date

09/03/2004

Pubmed ID

15341059

Scopus ID

2-s2.0-3142676341 (requires institutional sign-in at Scopus site)   1 Citation

Abstract

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.

Author List

Solenkova NV, Maslov LN, Serebrov VIu, Lishmanov AIu, Bogomaz SA, Gross GJ, Grover GJ

MESH terms used to index this publication - Major topics in bold

Adenosine Triphosphate
Animals
Electric Stimulation
Heart
Myocardial Infarction
Myocardium
Potassium Channel Blockers
Potassium Channels
Rats
Rats, Wistar
Sclerosis
Ventricular Fibrillation