[Involvement of central and peripheral cholinergic structures in regulation of cerebral electric activity and cardiac function in rabbits during hypoxia].

In the normoxic conditions, prior to the "ascent" of rabbits, the i.v. injection of M-choline blocking benactyzine slowed down the ECG rhythm already within the next few minutes. Irritation of the reticular formation against this background did not initiate the reaction of activation; yet, heart rate was essentially unaltered by benactyzine. This was ascribed to low effectiveness of the benactyzine M-cholinergic mediation with respect to the cardiac function in contrast to the electric activity of the brain cortex due to, apparently, the abundance of M-choline receptors in this structure. The effect of N-cholinolytic ganglerone on the spontaneous and induced cortical activities was weak and, as compared with benactyzine, more expressed upon the heart rate. These choline blockers combined with hypoxia and the benactyzine-produced slow ECG waves on the initial phase (4000-5000 m) brought about neither spontaneous nor induced by the reticular formation irritation activation of ECG. At the maximal "altitude" (8500-9000 m) the benactyzine-synchronized ECG rhythm tended to become deeper assuming the low delta-type activity observed at the same "altitude" without i.v. benactyzine. With this ECG, irritation of Dieters' formation was impotent to trigger the reaction of activation.