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PubMed1965

[Analytical study of anticholinergics from the group of carboxylic acid esters. VI. Study of the stability of the chloride of the beta-diethylaminoethylester of diphenylhydroxyacetic acid (benactyzine), of the chloride of the beta-diethylaminoethylester of the phenyl-n-propylacetic acid (prospasmine), of the 2-(phenylcyclohexylhydroxyacetoxy)-ethyl-dimethyldulfonium iodide (hydroxythiospasmine) and of the 2-(phenylcyclohexylacetoxy)-ethyldimethylsulfonium iodide (thiospasmine)].

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Benactyzine↗
PubMed1992

Behavioral effects of some diphenyl-substituted antimuscarinics: comparison with cocaine and atropine.

To more fully characterize the behavioral excitatory effects observed with certain diphenyl-substituted antimuscarinics, various behavioral effects of benactyzine, a prototype excitatory antimuscarinic, was evaluated in rats. These effects were compared to those of cocaine, atropine, and azaprophen, a muscarinic antagonist that contains both the diphenyl substituents of benactyzine and a ring isomeric with the tropane ring of atropine. Under a fixed-interval 5-min schedule of food presentation, cocaine and benactyzine increased response rates. Atropine and azaprophen only decreased responding. The muscarinic agonist oxotremorine attenuated the rate-increasing effects but did not alter the disruptions in the temporal patterning produced by benactyzine or shift the dose-effect function to the right. In rats discriminating 10 mg/kg cocaine from saline, benactyzine partially substituted for cocaine, producing a maximum of 50% cocaine-appropriate responses. Benactyzine fully substituted for scopolamine in rats discriminating 0.056 mg/kg scopolamine from saline. All antimuscarinics increased locomotor activity when activity levels were low in control animals, but the increases were less than those produced by cocaine. Cocaine increased both locomotor activity and fixed-interval responding at comparable doses, whereas 10-fold higher doses of benactyzine were required to increase locomotor activity. These results support the following conclusions: 1) In addition to its classical antimuscarinic behavioral profile, benactyzine has behavioral excitatory actions similar in some respects to those of cocaine; 2) the behavioral excitatory effects of benactyzine do not appear to be due solely to antagonism of muscarinic receptors; and 3) the alkyl-ester may be an important structural feature of diphenyl-substituted antimuscarinics for the induction of behavioral stimulation.

Animals↗
PubMed1977

[Contractile responses of the guinea pig ileal longitudinal muscle to antispasmodics (author's transl)].

Papaverine, benactyzine and Aspaminol were found to induce strong contractions of guinea pig ileal longitudinal muscle in a medium containing 3.2 mM of Ca2+. The contractile actions of papaverine, benactyzine and Aspaminol were potentiated with increase in Ca2+. The contractile actions of papaverine, benactyzine and action of papaverine was completely blocked by Mn2+, which by itself caused a contraction of the longitudinal muscle. The maximal contraction by papaverine was obtained at the concentration of more than 10(-5) M, WHILE BOTH BENACTYZINE AND Aspaminol induced the maximal contractions at the concentration of 3 X 10(-4) M. During and after the contraction by papaverine, contractile responses to benactyzine and Aspaminol were not observed. Changes in the intracellular level of cyclic GMP after exposure of the longitudinal muscle to papaverine, benactyzine or Aspaminol did not occur. These results suggest that papaverine, benactyzine Aspaminol may induce contractions of the ileal longitudinal muscle through a similar mechanism of action. A likely assumption is that these drugs move intracellular bound Ca2+ to the contractile protein of the muscle.

Acetylcholine↗
PubMed1999

[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.

Animals↗
PubMed1983

Efficacy and toxicity of drug combinations in treatment of physostigmine toxicosis.

Atropine, in combination with 1 of 6 other drugs, was tested in mice for the ability to prevent death by an otherwise lethal dose of the cholinesterase inhibitor, physostigmine. The atropine dose (4 mg/kg, i.p.) was kept constant, while the dose of the other drug in the pair was tested in 5 geometrically spaced doses, ranging down to 1/16 of the maximum dose (which caused no gross behavioral signs). Atropine alone saved 20% of the mice. The combination of atropine and benactyzine saved 100% of the mice at all 5 doses of benactyzine; similar complete protection was afforded by the combination of atropine and the largest dose of an oxime, TMB4 (15 mg/kg). Over 80% survivals were achieved with the larger doses of atropine combinations involving hexamethonium, mecamylamine, and diazepam. No enhanced protection occurred with atropine combinations with the oxime, 2-PAM. The toxicity of the effective combinations, when used in high doses without physostigmine challenge, revealed that deaths occurred over a narrow range of doses of all combinations except atropine/diazepam. An additive toxic effect of atropine was suggested with its combinations with TMB4, mecamylamine, and diazepam, whereas no additive toxicity occurred with combinations involving hexamethonium or benactyzine (i.e., the LD50 of the combinations was about the same as for hexamethonium or benzactyzine alone). The combinations with the best therapeutic safety ratio were with diazepam (no deaths at a dose 10 times that which saved 100% of mice) and benactyzine (no deaths at a more than 50-fold dose).

Animals↗
PubMed2003

Effect of methoxime combined with anticholinergic, anticonvulsant or anti-HCN drugs in tabun-poisoned mice.

The effect of methoxime combined with a) atropine, b) benactyzine, c) atropine and natrium thiosulphate, d) atropine and diazepam on antidotal treatment effectiveness was studied in tabun-poisoned mice. In addition, the influence of pretreatment consisiting of pyridostigmine, benactyzine and trihexyphenidyle (PANPAL) administered 2 hours before tabun intoxication on the treatment effectivity of methoxime combined with e) atropine or f) benactyzine was tested. The most efficacious therapeutic mixture in non-pretreated mice was methoxime, atropine and diazepam. Natrium thiosulphate did not significantly increase neither decrease the antidotal treatment efficacy in comparison with methoxime and atropine alone. Pretreatment with PANPAL significantly decreased tabun toxicity (nearly 4 times in methoxime and benactyzine combination and more than 4 times in atropine and methoxime mixture). The present study demonstrates that the tabun toxicity in mice is more effectively reduced when PANPAL prophylactically is administered than in case of treatment with methoxime and cholinergic drug alone. We established that anticholinergic drug option in the therapeutic mixture of methoxime and anticholinergic drug did not cause the difference in the antidotal treatment effectivities.

Animals↗