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J W HOWARD

Publications and source records attributed to J W HOWARD.

11 recordsLinked to original sources

Reciprocal potentiating action of depolarizing drugs on the isolated frog rectus abdominis muscle.

Subthreshold concentrations of the depolarizing agents, acetylcholine and decamethonium, potentiated isotonic contractures of the isolated frog rectus abdominis muscle elicited by effective doses of either of these drugs or by choline in the absence of the anticholinesterases, sarin, or dyflos. Comparable potentiation of the contracture produced by decamethonium or choline could be obtained by alternate stimulation with acetylcholine in the absence of dyflos or sarin. Furthermore, dyflos alone did not effect potentiation in the absence of alternate stimulation with acetylcholine. Finally, the inhibitory action of tubocurarine, as measured by depression of the contracture elicited by decamethonium and acetylcholine, was not antagonized by sarin. It was concluded that the enhancement of the response to acetylcholine produced by dyflos and by sarin was brought about exclusively by their action as inhibitors of cholinesterase. The ability of dyflos and of sarin to potentiate contractures elicited by decamethonium or by choline may be attributed to a facilitation of the action of the depolarizing compounds by subthreshold concentrations of acetylcholine available in the presence of these anticholinesterases.

Acetylcholine↗

Effect of pyridine aldoximes on response of frog rectus muscle to acetylcholine.

The effects of pyridine-2, 3- and 4-aldoxime methiodide (PAM) on the isotonic contracture of the isolated frog rectus abdominis muscle elicited by acetylcholine have been studied. The potentiation to acetylcholine resulting from incubation with PAM isomers is reversible and may be related to the weak anticholinesterase property of these compounds. Concentrations of the isomers higher than those needed for maximal potentiation produce a reversible block of the muscle to acetylcholine. pH studies suggest that cations are responsible for the potentiating and blocking properties of the PAM isomers.

Acetylcholine↗

Potentiation of the response of frog rectus muscle to acetylcholine by isopropyl methyl phosphonofluoridate and its modification by pyridine-2-aldoxime methiodide.

Pyridine-2-aldoxime methiodide (P2AM) was used to study the relation between the recovery of cholinesterase activity of isolated frog rectus abdominis muscle and the change of isotonic response to acetylcholine after previous treatment with the anticholinesterase, isopropyl methyl phosphonofluoridate (sarin). Addition of P2AM to muscle which had been incubated with sarin produced an 88% decrease in potentiation to acetylcholine. This was accompanied by 71% and 35% recoveries of the cholinesterase activity of the intact and finely ground muscle respectively compared with controls from the contralateral muscle. Following pre-treatment with sarin, a two-hour rinsing with acetylcholine (3 mug./ml.) produced a 61% decrease in potentiation to acetylcholine accompanied by 24% and 4.5% recoveries of cholinesterase activity in intact and in ground muscle respectively. Since control experiments showed absence of uncombined sarin in the muscle after rinsing with acetylcholine solution, the results indicate a greater effectiveness of P2AM and acetylcholine in reactivating superficially situated cholinesterase of the frog rectus abdominis as compared with enzyme within the interior of the muscle.

Acetylcholine↗

Dextran.

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Dextrans↗