[The effect of K(ATP)-channel activation on the electrical stability of myocardium in rats with postinfarction cardiosclerosis].

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.

• Authors: N V Solenkova, L N Maslov, V Iu Serebrov, A Iu Lishmanov, S A Bogomaz, G J Gross, G J Grover
• Journal: Eksperimental'naia i klinicheskaia farmakologiia (Eksp Klin Farmakol) 2004 May-Jun Vol. 67 Issue 3 Pg. 10-3 ISSN: 0869-2092 [Print] Russia (Federation)
• Vernacular Title: Vliianie aktivatsii K(ATP)-kanalov na élektricheskuiu stabil'nost' miokarda pri postinfarktnom kardioskleroze.
• PMID: 15341059 (Publication Type: English Abstract, Journal Article, Research Support, U.S. Gov't, P.H.S.)

Chemical References

• Potassium Channel Blockers
• Potassium Channels
• Adenosine Triphosphate

Topics

• Adenosine Triphosphate (physiology)
• Animals
• Electric Stimulation
• Heart (physiopathology)
• Myocardial Infarction (complications, pathology)
• Myocardium (pathology)
• Potassium Channel Blockers (pharmacology)
• Potassium Channels (drug effects, physiology)
• Rats
• Rats, Wistar
• Sclerosis (etiology)
• Ventricular Fibrillation (etiology, physiopathology)