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W Bak

Publications and source records attributed to W Bak.

13 recordsLinked to original sources
PubMed1981

Adaptation of the neuromuscular junction to chronic acetylcholinesterase inhibition due to phospholine treatment.

The disturbances of neuromuscular transmission due to chronic (1 to 30 days) administration of phospholine to rats were investigated upon the isolated diaphragm preparation. Phospholine treatment impaired the ability of the muscle to maintain tetanic contraction in response to indirect stimulation and caused post-tetanic depression of twitch responses. In the later stage marked recovery of neuromuscular function occurred in spite of further phospholine administration. This recovery was not accompanied by any increase in the already lowered acetylcholinesterase activity. The concentration of d-tubocurarine needed to block twitch response increased during the first days of phospholine treatment and then, during the following period gradually returned to the normal level. The concentration of carbachol needed to block twitch response during 2 to 30 days of continued treatment was higher than that in control animals. The possible explanations for the spontaneous recovery of neuromuscular function are discussed.

Animals↗
PubMed1977

Central anticholinergic effects of N-ethyl-2-pyrrolidylmethyl-cyclopentylphenyl glycollate.

The following effects of N-ethyl-2-pyrrolidyl-methyl-cyclopentylphenyl glycollate (PMCG) have been studied: effects on aggressive behaviour in mice and on general behaviour in rats, protective effects against central action of arecoline and nicotine in mice, thermo-regulatory effects in mice, protective action in poisonings with fluostigmine in mice and rats, and effects on bioelectrical activity of the brain in cats. It was stated that PMCG possesses a strong central anticholinergic activity blocking predominantly central muscarinic receptors; PMCG had also strong protective effects in anticholinesterase intoxications. It is suggested that this drug could have antiemotional and antiparkinsonian properties.

Aggression↗
PubMed1976

Therapeutic effects of some cholinolytics in organophosphate intoxications.

The therapeutic effects of pipethanate (sycotrol) and two newly synthetized cholinolytics, DPX-8 and ANC-51, were compared with atropine in mice poisoned by DDVP, fluostigmine, phospholine, and paraoxon. The antagonistic activotagonistic activity of tested drugs against acetylcholine-induced contraction of rat ileum and oxotremorine-induced salivation and tremor in the mouse was also studied. The anticholinergic activity of pipethanate, DPX-8, and ANC-51 was weaker than that of atropine. However,the therapeutic effect of pipethanate was higher than that of atropine in mice poisoned by the organophosphates. DPX-8 and ANC-51 afforded a better antidotal effect than atropine only in DDVP-poisoned mice.

Animals↗
PubMed1976

Efficacy of repeated pharmacotherapy in experimental acute poisonings with fluostigmine.

The effectiveness of repeated pharamacotherapy in acute poisonings with fluostigmine was studied in rats. It was demonstrated, that the second i.p. administration of obidoxime (40 mg/kg) was without effect. Repeated i.p. administration of atropine (10 mg/kg) shown marked efficacy only in animals treated previously with atropine (10 mg/kg) and diazepam (2.5 mg/kg). This procedure was without effect in animals treated just after intoxication with atropine (10 mg/kg) or atropine (10 mg/kg) and obidoxime (40 mg/kg). Subsequent administration of diazepam (2.5 mg/kg) or caramiphen (10 mg/kg) was without effect.

Animals↗
PubMedDate not supplied

Adaptation of neuromuscular junction to transmission of impulses after inactivation of acetylcholinesterase.

Adaptation of neuromuscular junction to transmission of impulses after inactivation of acetylcholinesterase. Acta Physiol. Pol., 1977, 28 (1): 23-30. Isolated preparation of rat diaphragm with phrenic nerve was incubated in paraoxon solutions which caused complete inactivation of acetylcholinesterase. This inactivation was associated with disturbances of neuromuscular transmission in the form of blockade of the tetanic response, post-tetanic inhibition of twitch responses and a decreased amplitude of the second response after the first one when two stimuli at a short interval were used. These disturbances were withdrawn somewhat during further incubation of the preparation, although it was kept in paraoxon solution which maintained complete inactivation of acetylcholinesterase. It is suggested that the observed recession of transmission disturbances may be caused by partial adaptation of blockade of the tetanic response, post-tetanic inhibition of twitch blockade of enzymatic hydrolysis of acetylcholine.

Acetylcholinesterase↗
PubMedDate not supplied

Neuromuscular function in fluostigmine intoxication.

In experiments with isolated nerve-diaphragm preparation and intact anterior tibial muscle of the rat, it was found that repeated administration of fluostigmine (1 to 30 days) caused a decrease of the indirectly elicited tetanic response and post-tetanic depression of twitch response. Impairment of neuromuscular transmission increased during the first days of treatment. In the following period marked recovery occurred in spite of further fluostigmine administration. The recovery of neuromuscular function was much more pronounced in diaphragm preparation than in the anterior tibial muscle. It was not associated with any recovery in the activity of inhibited acetylcholinesterase. The sensitivity of the neuromuscular junction to carbachol increased during the first days of treatment and then decreased in the later stage. The sensitivity to d-tubocurarine in the diaphragm preparation decreased on the tenth day of treatment and returned to normal value after 30 days. In the anterior tibial muscle the sensitivity to d-tubocurarine slightly decreased on the fifth day, and after 20 to 30 days, was markedly increased. The underlying mechanisms are discussed.

Acetylcholinesterase↗