Autor: |
Kryzhanovskii SA; V. V. Zakusov Research Institute of Pharmacology, Russian Academy of Sciences, Moscow, Russia. SAK_538@yandex.ru., Kozhevnikova LM; Research Institute of General Pathology and Pathological Physiology, Russian Academy of Medical Sciences, Moscow, Russia., Tsorin IB; V. V. Zakusov Research Institute of Pharmacology, Russian Academy of Sciences, Moscow, Russia., Sukhanova IF; Research Institute of General Pathology and Pathological Physiology, Russian Academy of Medical Sciences, Moscow, Russia., Ionova EO; V. V. Zakusov Research Institute of Pharmacology, Russian Academy of Sciences, Moscow, Russia., Stolyaruk VN; V. V. Zakusov Research Institute of Pharmacology, Russian Academy of Sciences, Moscow, Russia., Vititnova MB; V. V. Zakusov Research Institute of Pharmacology, Russian Academy of Sciences, Moscow, Russia., Miroshkina IA; V. V. Zakusov Research Institute of Pharmacology, Russian Academy of Sciences, Moscow, Russia., Seredenin SB; V. V. Zakusov Research Institute of Pharmacology, Russian Academy of Sciences, Moscow, Russia. |
Abstrakt: |
Original translational rat model of chronic heart failure provoked by experimental anterior transmural myocardium infarction was employed to examine the preventive action of anxiolytic Afobazole (15 mg/kg/day administered intraperitoneally during the first 15 days after coronary occlusion) on the development of the heart failure assessed in 3 months after infarction. Afobazole prevented the development of pathologic remodeling of the myocardium, maintained its inotropic function, and decreased the plasma level of brain natriuretic peptide known as a biochemical marker of chronic heart failure. In the myocardium, Afobazole down-regulated overexpression of the genes induced in chronic heart failure and assessed by corresponding RNA levels, which code angiotensin (AT1A-R), vasopressin (V1A-R), and glucocorticoid (GR) receptors as well as Epac2 protein. The revealed biochemical changes are consistent with the data on cardioprotective action of Afobazole. |