Effects of halothane on acetylcholine release and sympathetic ganglionic transmission

Abstract

Depression of synaptic transmission is one of the actions common to many general anesthetics. They appear to act primarily on the chemical transmission process itself without affecting the conduction of impulses in nerve axons. The objective of the present study was to directly examine the effects of halothane on the release of acetylcholine and overall ganglionic transmission. The effects of halothane on ganglionic transmission were studied in the stellate ganglion of the cat in vitro. The preganglionic nerves of the stellate ganglion were stimulated electrically to generate threshold and suprathreshold evoked potentials in the postganglionic nerves. The picomole levels of released acetylcholine in the superfusate were determined with a radioenzymatic method using 32P-ATP following a 5-min preganglionic stimulation before and after the addition of 0.28 and 0.59 mM halothane (vaporizer settings of 1% and 2%, respectively). Halothane at both concentrations: 1) depressed sympathetic ganglionic transmission induced by either threshold or suprathreshold stimulation of the preganglionic nerves; and 2) caused a dose-dependent decrease in acetylcholine release during threshold stimulation with no change in neurotransmitter release during suprathreshold stimulation. In summary, the interruption of synaptic transmission by halothane involves at least two mechanisms: 1) decrease in acetylcholine release during low level of synaptic transmission; and 2) postsynaptic decrease in sensitivity to acetylcholine during low and high levels of synaptic transmission.