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In order to evaluate the effect of an opioid antagonist on depressed intrinsic central vaso-motor drive (carotid sinus reflex) and high voltage slow delta waves in the EEG associated with halothane, naloxone was injected intravenously in a bolus of 100 or 200 micrograms.kg-1 on different days in the anaesthetized dog (0.64 Vol% halothane in oxygen). Only the 200 micrograms.kg-1 dose of naloxone reversed the halothane-induced depression of the blood pressure and heart rate response to clamping of both exteriorized common carotid arteries. The EEG changed from high voltage slow waves to low voltage fast waves, inducing a reduction of power in the delta band in spectral analysis. This effect was most pronounced during the 20th minute post naloxone injection. Naloxone did not reverse the halothane-related hypotension and bradycardia. Because of the late "cortical arousal" reaction during halothane-anaesthesia and the high dose necessary, naloxone appears to exert its action through a generalized increase in CNS excitation. An antagonisation of halothane-induced release of opiate-like peptides therefore is less likely.

Naloxone reverses the hypnotic effect and the depressed baroreceptor reflex of halothane anaesthesia in the dog