Pancuronium increases the duration of electroencephalogram burst suppression in dogs anesthetized with isoflurane

Earlier studies have demonstrated both a decrease as well as no effect on halothane MAC after administration of nondepolarizing neuromuscular relaxants. To clarify further the relationship between neuromuscular blocking agents and anesthetic potency, the authors studied the effect of pancuronium on steady-state electroencephalogram (EEG) burst suppression produced by isoflurane in dogs. Anesthesia was induced using isoflurane and oxygen via mask without the administration of other drugs. The trachea was intubated, and isoflurane was administered at a concentration sufficient to produce EEG burst suppression. Thereafter, end-tidal isoflurane concentration, temperature, and end-tidal P(CO₂) were meticulously maintained at constant values. Dogs in group 1 (n = 6) received pancuronium 0.1 mg · kg^-1. The percent of the EEG that was isoelectric increased from 21 ± 9% (mean ± SD) to 35 ± 11% (P < 0.01). After the return of single-twitch response to train- of-four stimulation, neostigmine 0.05 mg · kg^-1 and glycopyrrolate 0.01 mg · kg^-1 were administered. This resulted in a reduction in EEG isoelectricity to 19 ± 8% (P < 0.01), similar to the value before pancuronium administration. In group 2 dogs (n = 6), the percent isoelectricity of the EEG prior to pancuronium was 25 ± 10%. After administration of pancuronium 0.02, 0.04, and 0.2 mg · kg^-1 sequentially, the percent isoelectricity of the EEG was 29 ± 11, 37 ± 15, and 43 ± 9%, respectively. This represents a dose-related increase in isoelectricity for the 0.04- and 0.2-mg · kg^-1 doses (P < 0.05). The increased duration of isoelectricity during isoflurane EEG burst suppression resulting from pancuronium administration indicates that the effect of isoflurane on the brain is enhanced by nondepolarizing neuromuscular blockade.