Article date: December 1973
By: M. H. EVANS, PAMELA J. JAGGARD in Volume 49, Issue 4, pages 651-657
Dimethyl sulphoxide (DMSO) partially reversed neuromuscular blockade brought about by the action of (+)‐tubocurarine or Mg2+ on the frog sartorius nerve‐muscle preparation.
The amplitude and duration of the endplate potential (e.p.p.) were increased by DMSO at concentrations of 70 mm or greater.
Miniature endplate potentials were raised in frequency, prolonged in duration and increased in amplitude by DMSO at concentrations of 141 mm or greater, but the increase in amplitude was generally less than in the case of the e.p.p.
The resting muscle membrane potential was significantly depolarized by DMSO at 70 mm or greater concentrations, both at the endplate and remote from an endplate.
The reversal of neurmuscular blockade by DMSO can be explained in terms of its previously reported ability to inhibit cholinesterase activity, together with the depolarizing action on muscle.
Dimethyl sulphoxide (DMSO) partially reversed neuromuscular blockade brought about by the action of (+)‐tubocurarine or Mg2+ on the frog sartorius nerve‐muscle preparation.
The amplitude and duration of the endplate potential (e.p.p.) were increased by DMSO at concentrations of 70 mm or greater.
Miniature endplate potentials were raised in frequency, prolonged in duration and increased in amplitude by DMSO at concentrations of 141 mm or greater, but the increase in amplitude was generally less than in the case of the e.p.p.
The resting muscle membrane potential was significantly depolarized by DMSO at 70 mm or greater concentrations, both at the endplate and remote from an endplate.
The reversal of neurmuscular blockade by DMSO can be explained in terms of its previously reported ability to inhibit cholinesterase activity, together with the depolarizing action on muscle.
DOI: 10.1111/j.1476-5381.1973.tb08540.x
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