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Results for “Decamethonium Compounds”

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At least 595 records · Page 33Linked to original sources
PubMed1984

Effects of neuromuscular blocking agents and acetylcholinesterase inhibitors on the response of pectoral fin muscle of the sculpin (Enophrys bison) to indirect stimulation.

The neuromuscular junction of the buffalo sculpin (Enophrys bison) was characterized in situ by examining the effects of various neuromuscular blocking agents and acetylcholinesterase inhibitors (ACHE-I) on pectoral muscle response to indirect stimulation. The injection of either d-tubocurarine (350 micrograms/kg) or alpha-bungarotoxin (alpha-Butx) (1 mg/kg) resulted in a flaccid paralysis. The depolarizing agents, succinylcholine (11 micrograms/kg) and decamethonium (42 micrograms/kg), produced a spontaneous contraction. The administration of the ACHE-I, diisopropyl fluorophosphate (DFP), and eserine resulted in responses which were contrary to those expected based on similar experiments using mammalian skeletal muscle. Twitch potentiation did not occur and the ability to maintain a tetanic response was not abolished even after the administration of clearly lethal concentrations of ACHE-I.

Acetylcholinesterase↗
PubMed1975

[The blocking action of snake venom polypeptides on the cholinergic mechanisms of leech dorsal muscle].

The blocking action of alpha-polypeptides from the venoms of elapid snakes (Bungarus multicinctus and Naja naja siamensis) was studied on leech dorsal muscle. It was shown that these neurotoxins failed to inhibit the responses to mononitrogen cholinomimetics (acetylcholine, nicotine, carbamylcholine, etc.). The capacity of neurotoxins to inhibit the responses to the bisquaternary cholinommimetics depended upon the length of the molecule. The neurotoxins were active against the "shorter" cholinomimetics, such as decamethonium, and bischolinic esters of malonic, succinic and glutaric acids. The "longer" cholinomimetics (bischolinic esters of adipinic, pimelic, suberic, azelaic, sebacic acids retained their full activity after the treatment of leech dorsal muscle by neurotoxins. Possible explanations of the selective action of neurotoxins are discussed.

Acetylcholine↗
PubMed1975

Quantitative extraction of tubocurarine, gallamine, and decamethonium from biological materials.

A procedure is described for quantitative extraction of tubocurarine, gallamine, and decamethonium from blood, urine, and tissue. Ion pairs of the drugs are formed with picric acid and are extracted into a dichloromethane/1-pentanol solvent. Qualitative analysis of the extract is effected using thin-layer chromatography. Quantitative analysis is accomplished by elution of TLC areas containing the drug, formation of the ion pair with sodium 9,10-dimethoxyanthracene-2-sulfonate, and analysis of the ion pair by spectrophotofluorometry.

Anthracenes↗
PubMed2001

The Effects of isoflurane on acetylcholine receptor channels: 3. Effects of conservative polar-to-nonpolar mutations within the channel pore.

We performed macroscopic and single-channel current measurements on wild-type (WT) and two mutant muscle-type nicotinic acetylcholine (ACh) receptor channels transiently expressed in HEK-293 cells. The mutants contained polar-to-nonpolar substitutions at the 10' (alpha(2)S10'A beta T10'A gamma delta) and 6' positions (alpha(2)S6'A beta gamma delta S6'A) in the M2 pore region of the channel. We studied the behavior of these channels in the absence and presence of the volatile general anesthetic isoflurane. Both mutations changed the gating behavior of the channel. A comparison of the alpha(2)S10'A beta T10'A gamma delta mutant to WT receptors revealed faster desensitization kinetics, increased sensitivity to ACh, a higher efficacy for activation by the partial nicotinic agonist decamethonium, and a greater number of openings per burst. A comparison of the alpha(2)S6'A beta gamma delta S6'A mutant to WT receptors also revealed increased sensitivity to ACh and an increased burst duration at the single-channel level with ACh as agonist. The alpha(2)S10'A beta T10'A gamma delta mutation increased the sensitivity of the ACh receptor to isoflurane, whereas the alpha(2)S6'A beta gamma delta S6'A mutation did not. These changes were probably not caused by the differential effects of the mutation on channel gating and desensitization. The increased sensitivity of the alpha(2)S10'A beta T10'A gamma delta receptor to isoflurane is state-dependent; the mutation changes the affinity of the closed state but not that of the open state of the channel.

Anesthetics, Inhalation↗
PubMed1975

[Changes in the mitotic regime of cultures of continuous human amniotic cells (line A1) subjected to the action of decamethoxin].

The effect of decamethoxin solutions on the cultures of the permanent line of the amniotic human cells (A1) was studied. In concentrations of 1000 and 50-500 gamma/ml decamethoxin induced fixation of the cell layer and destruction of cells A1 respectively. Higher dilutions of decamethoxin from 10 to 0.1 gamma/ml induced suppression of the mitotic activity and arrest of the cells in the telophase. Possible causes of the changes in the mitotic regimen are discussed. Therefore, decamethoxin slackened the cell dividing process in vitro and blocked passage of the cells from the telophase into period G1 of the interphase.

Amniotic Fluid↗