Abstract

Streptomycin possesses neuromuscular blocking properties. When injected intravenously in the dose of 110 mgm. per kgm. of body weight, the contractions of the tibialis anticus indirectly stimulated with shock delivered at a rate of 50 per minute were abolished in some dogs. In others, streptomycin reduced markedly the amplitude of the tibialis anticus contractions. When administered in larger doses, streptomycin induced complete myoneural blockade to tetanizing impulses. The muscle responded always to direct stimulation. Nerve tetanization, neostigmine and calcium were shown to antagonize streptomycin blockade.

Under neuromuscular blockade produced by streptomycin and that produced by magnesium, some effects such as the response to tetanic indirect stimulation when isolated volleys of impulses are blocked, post-tetanic facilitation, the responses to tetanic stimulation of the nerve during progressive neuromuscular blockade and the effect of calcium chloride administration are surprisingly alike. This seems to suggest the same mechanisms of action in both cases.

On intact unanesthetized dogs and pigeons, streptomycin induced muscular hypotonia, flaccid paralysis and vomiting. Calcium and neostigmine suppressed the motor effects of the acute streptomycin intoxication.

The motor signs of the acute streptomycin poisoning should be imputed to neuromuscular blockade since neostigmine abolished them. Death of the animals, dogs and pigeons, should be also attributed to the neuromuscular blocking action of streptomycin.