Delayed Contraction of Denervated Muscle with Intravenous Barbiturates. ∗

Abstract

It is a known fact that denervated striated muscle contracts when in contact with cholinergic substances that have nicotinic properties. Intravenous injections of minute doses of acetylcholine and certain carbominocholine derivatives produce a contraction of denervated facial muscles within the circulation time. 1 Large doses of epinephrine also cause the denervated facial muscle to contract, but this does not occur until 60 to 90 seconds after the intravenous injection. Such delayed muscular contraction is probably the result of a secondary, rather than direct effect of epinephrine. 2

In the course of these experiments, it was noted that intravenous sodium pentobarbital anesthesia produced a delayed contraction of the denervated facial muscle in 11 of 12 tested monkeys. The contraction appeared after a latency varying from 16 to 60 seconds following the administration of 25 mg of sodium pentobarbital per kilo of body weight. The contraction could be elicited only by the intravenous route with a speed of not less than 10 mg per second. So long as the injection was rapid, the effect could be obtained even with subanesthetic doses.

The contraction induced with sodium pentobarbital lasted from 40 to 75 seconds. It could be so elicited so long as the muscle remained denervated. It was slightly enhanced by eserine and never blocked by atropine.

Similar results, and under the same conditions, were obtained with other barbiturates, such as sodium thiopentobarbital, sodium amytal, and sodium evipal. Intravenous injection of other anesthetics, such as paraldehyde, urethane, or ether inhalation did not produce contraction in the denervated face.

The mechanism of this contraction is difficult to explain. Barbiturates have no significant direct stimulation effect on striated muscle in vitro. 3 This, and the fact the contraction is delayed, suggest that the effect is indirect and secondary.