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.

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.

No abstract

The risk of appearance of non-motor symptoms including cognitive dysfunctions is increased while Parkinson's disease (PD) progression. A lot of EEG-studies have shown that the degree of cognitive impairments correlates with increasing of θ-band spectral power. The aim of this research was to investigate the cause of such phenomenon. The resting state EEGs of 30 patients with PD and 30 healthy volunteers 45-65 years old were analyzed. We have established that the increasing of θ power has heterogenic nature. First reason is greater activity of existing θ-generators, mainly in posterior cingulate cortex. The other reason is the decreasing of the dominant resting state rhythm's frequency, which can affect the values of spectral power of θ-band.