RESUMO
Seven-day treatment of rats with experimental myocardial infarction with afobazole (5-ethoxy-2-[2-morpholino)-ethylthio] benzimidasole dihydrochloride) resulted in shrinkage of the ischemic damage area in the heart, stimulation of reparative processes in the myocardium, and prevention of postinfarction remodeling of the left ventricle. Anti-ischemic effect of afobazole in experimental myocardial infarction is presumably due to its interactions with σ(1) receptors.
Assuntos
Benzimidazóis/farmacologia , Benzimidazóis/uso terapêutico , Morfolinas/farmacologia , Morfolinas/uso terapêutico , Infarto do Miocárdio/tratamento farmacológico , Miocárdio/metabolismo , Remodelação Ventricular/efeitos dos fármacos , Animais , Proliferação de Células/efeitos dos fármacos , Masculino , Infarto do Miocárdio/patologia , Miocárdio/citologia , Ratos , Receptores sigma/metabolismo , Estatísticas não ParamétricasRESUMO
Effect of afobazole on the threshold of electrical fibrillation of the heart was studied on anesthetized rats with intact myocardium. It was shown that the drug considerably increased the threshold of electrical fibrillation of the heart, being not inferior to reference class I antiarrhythmic drugs (lidocaine and procainamide) according to V. Williamse classification. Against the background of preliminary injection of σ-receptor antagonist haloperidol, afobazole exhibited no antifibrillatory activity. These findings and analysis of published reports suggest that antifibrillatory activity of afobazole is determined by its antagonistic influence on σ1-receptors localized in cardiomyocyte cytosol.
