DIRECT COMPARATIVE EFFECTS OF ISOFLURANE AND DESFLURANE ON SYMPATHETIC GANGLIONIC TRANSMISSION

Although the sympathetic ganglion is an important site of peripheral regulation, few studies have examined the effect of anesthetics on synaptic transmission. In the present study we compared the actions of desflurane with those of isoflurane on synaptic transmission and neurotransmitter release in the stellate ganglion. In the electrophysiologic group, 14 stellate ganglia were isolated from adult mongrel dogs after halothane anesthesia, desheathed, and superfused with Krebs' solution. Compound action potentials (CAP) were induced by supramaximal stimulation of the preganglionic T3-ramus at a low frequency of 0.4 Hz and were recorded from the postganglionic ventral ansa subclaviae. Each ganglion was exposed to two levels of anesthetics (equivalent to 1 and 2 minimum alveolar anesthetic concentration [MAC]), followed by an anesthetic-free washout period. While equianesthetic concentrations of isoflurane and desflurane caused essentially equipotent suppression of ganglionic transmission, desflurane was more efficacious than isoflurane, both with respect to the onset of and recovery from the inhibition of synaptic activity. In the electrochemical group, 25 ganglia were exposed to both anesthetics at a high concentration (equivalent to between 1.82 and 1.95 MAC) during maximal and submaximal current stimulations, and the release of actylcholine (ACh) in the superfusate was measured with liquid chromatography. Although desflurane and isoflurane caused a significant depression of CAP, neither anesthetic inhibited the release of ACh in the superfusate at either maximal or submaximal current stimulations. These results indicate that the suppression of ganglionic activity is equipotent for both anesthetics based on equivalent MAC values, but that desflurane is more efficacious than isoflurane with respect to onset and recovery at the higher concentrations of anesthetics. The source of impaired conduction appears to be a reduced sensitivity to neurotransmitter release in the postsynaptic neuron.