Electroencephalographic Evidence of Arousal in Dogs from Halothane after Doxapram, Physostigmine, or Naloxone

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Abstract
The clinical impressions of enhanced arousal from halothane anesthesia and improvement of postanesthesia recovery scores after doxapram, phgysostigmine or naloxone have not been verified in laboratory studies based on the effect of these drugs on MAC [minimum anesthetics concentration]. With induction of anesthesia, a shift in the amplitude of the EEG from low to high occurs at anesthetic concentrations well below MAC and appears to coincide with the loss of consciousness. The effect of arousal agents on the end-tidal halothane concentration required to produce this shifting EEG was examined. In 24 unmedicated dogs, the end-tidal halothane concentration was elevated to 20% above the shift point concentration (from 0.61 .+-. 0.03 to 0.73 .+-. 0.03%) and maintained at this level for 30 min. Doxapram, 1 mg/kg, i.v. and physostigmine, 0.03 mg/kg, i.v., converted the EEG from a high amplitude to a low amplitude tracing in 22 .+-. 3 s in 8 of 8, and 225 .+-. 37 s in 7 of 8 dogs, respectively. The end-tidal halothane concentration required to restore the shifting EEG was elevated above control for 50 .+-. 7 and 109 .+-. 7 min, respectively. Naloxone, 0.06 mg/kg, i.v., produced an awake EEG in 2 of 8 dogs in 233 .+-. 18 s which persisted for 22 .+-. 4 min and a transiently shifting EEG in 3 of 8 dogs between 200-240 s. Naloxone 0.006, mg/kv, i.v., produced an awake EEG in 80 .+-. 8 s in 4 of 4 dogs who had previously received doxapram 3 h earlier. In this model, doxapram and physostigmine paralleled the clinically observed onset and duration of arousal. The inconstant arousal from halothane anesthesia induced by naloxone was interpreted in terms of an opiate receptor independent action.