N. Boban et al., DIRECT COMPARATIVE EFFECTS OF ISOFLURANE AND DESFLURANE ON SYMPATHETIC GANGLIONIC TRANSMISSION, Anesthesia and analgesia, 80(1), 1995, pp. 127-134
Although the sympathetic ganglion is an important site of peripheral r
egulation, few studies have examined the effect of anesthetics on syna
ptic transmission. In the present study we compared the actions of des
flurane with those of isoflurane on synaptic transmission and neurotra
nsmitter release in the stellate ganglion. In the electrophysiologic g
roup, 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 stimula
tion of the preganglionic T3-ramus at a low frequency of 0.4 Hz and we
re recorded from the postganglionic ventral ansa subclaviae. Each gang
lion was exposed to two levels of anesthetics (equivalent to 1 and 2 m
inimum alveolar anesthetic concentration [MAC]), followed by an anesth
etic-free washout period. While equianesthetic concentrations of isofl
urane and desflurane caused essentially equipotent suppression of gang
lionic 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 expos
ed 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 rel
ease of ACh in the superfusate at either maximal or submaximal current
stimulations. These results indicate that the suppression of ganglion
ic 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 anesthet
ics. The source of impaired conduction appears to be a reduced sensiti
vity to neurotransmitter release in the postsynaptic neuron.