| Autor: |
Solenkova NV, Maslov LN, Serebrov VIu, Lishmanov AIu, Bogomaz SA, Gross GJ, Grover GJ |
| Jazyk: |
ruština |
| Zdroj: |
Eksperimental'naia i klinicheskaia farmakologiia [Eksp Klin Farmakol] 2004 May-Jun; Vol. 67 (3), pp. 10-3. |
| Abstrakt: |
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. |
| Databáze: |
MEDLINE |
| Externí odkaz: |
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