The actions of neuromuscular relaxants at hyperbaric pressures.

Previous studies have shown that high pressures increase the twitch tension of directly or indirectly stimulated mammalian muscle, while depressing transmission at the neuromuscular junction. The present paper explores the interaction between high pressures and muscle relaxants on the indirectly stimulated rat phrenic nerve--diaphragm preparation. Two muscle relaxants, d-tubocurarine and succinylcholine, were studied. Measurements of the electromyogram and twitch tension amplitudes were made before and after application of the muscle relaxants and compared with results of measurements of those two variables under hyperbaric conditions. High pressures tended to enhance neuromuscular blockade by d-tubocurarine more than that by succinylcholine, as indicated by electromyographic suppression, and high pressures tended to antagonize the succinylcholine effect on twitch tension more than that of d-tubocurarine. The findings are in agreement with previous observations that high pressures increase muscular twitch tension and depress excitatory synapses. They further demonstrate a complex interaction between hyperbaric pressures and neuromuscular blocking drugs.

The depressant effect of halothane and sodium thiopental on the spontaneous and evoked activity of dorsal horn cells: lamina specificity, time course and dose dependence.

The effects of halothane and sodium thiopental on dorsal horn cell unit activity were studied in the lumbar spinal cord of decerebrate, low thoracic spinal cats. Both halothane (0.5, 1 and 1.5%) and sodium thiopental (2.5, 5 and 10 mg/kg) depressed, in a dose-dependent manner, the spontaneous firing frequency of cells in Rexed laminae I, V and VI and the evoked firing frequency of cells in laminae I and V. They, however, had no effect on cells in lamina IV. The maximum depression of cell activity occurred 5 to 8 minutes after inhalation of halothane and 2 to 3 minutes after the intravenous administration of sodium thiopental. The recovery of cell activity occurred within 15 to 30 minutes after discontinuation of halothane and within 10 to 30 minutes after intravenous administration of sodium thiopental. The depressive effect of halothane and sodium thiopental, both primarily hypnotic anesthetics, on lamina VI cells is in contrast to our previous finding that morphine sulfate, nitrous oxide and ketamine hydrochloride, primarily analgesic agents, had no significant effect on this lamina.