Keywords
Abstract
The aim of the study is to compare Bellastezin and atropine antispasmodic activity on a model of acetylcholine-dependent contractile activity (myogenic and neurogenic) of isolated strips of guinea pigs intestinal smooth muscles (ISM). The study was conducted on 10 guinea pigs male (weight 300–350 g). To exclude the possibility of benzocaine interfering effect on smooth muscle contractile responses, the extraction of alkaloids from the Bellastezin tablet mass was carried out in an aqueous solution, and only fractions of water-soluble substances were tested. Based on the general similarity of the mechanisms of action and physiological effects, the specific activity of Bellastezin was compared with atropine sulfate as reference test item. Bellastezin and atropine (10–9–10–6 M) administration into the chamber with ISM strips simultaneously with acetylcholine (10–6 M) caused a decrease in the amplitude and integral intensity of acetylcholinestimulated contractile activity of ISM. A significant change in the slope of Bellastezin concentration-effect curve (the Boltzmann equation) in comparison with atropine indicates that this drug differs from atropine in the nature of the antagonistic interaction with M-acetycholine receptors. Differences in the action of Bellastezin (10–10–10–7 M) revealed in the functional test, suggest that this medication at low concentration has influence on electrical stimulated ISM contractile responses rather like scopolamine (hyoscine) one, than atropine (hyoscyamine). Under dose-dependent acetylcholine-stimulated contractile activity of ISM, Bellastezin caused a significant shift to the right concentration-effect curves, in comparison to atropine moderate effect. Along with a significant decrease in the sensitivity of ISM to the action of acetylcholine, this medication also reduced maximal response amplitude, unlike atropine. The results suggest that natural mixture of alkaloids (Bellastezin) caused stronger and complex effects than atropine as for elimination of functional responses caused by M-acetylcholine receptors stimulation.