METHODS: Dogs were anesthetized with sevoflurane on two occasions, 1 week apart, and baseline MAC(BAR) (B-MAC(BAR)) was determined on each occasion. MAC(BAR) was defined as the mean of the end-tidal sevoflurane concentrations that prevented and allowed an increase (≥15%) in heart rate or invasive mean arterial pressure in response to a noxious electrical stimulus (50 V, 50 Hz, 10 ms). Dogs then randomly received either a low-dose (LDS) or high-dose series (HDS) of ketamine, and treatment MAC(BAR) (T-MAC(BAR)) was determined. The LDS had an initial loading dose (LD) of 0.5 mg kg(-1) and constant rate infusion (CRI) at 6.25 μg kg(-1) minute(-1), followed, after T-MAC(BAR) determination, by a second LD (1 mg kg(-1)) and CRI (12.5 μg kg(-1) minute(-1)). The HDS had an initial LD (2 mg kg(-1)) and CRI (25 μg kg(-1) minute(-1)) followed by a second LD (3 mg kg(-1)) and CRI (50 μg kg(-1) minute(-1)). Data were analyzed with a mixed-model anova and are presented as LSM ± SEM. RESULTS: The B-MAC(BAR) was not significantly different between treatments. Ketamine at 12.5, 25, and 50 μg kg(-1) minute(-1) decreased sevoflurane MAC(BAR), and the maximal decrease (22%) occurred at 12.5 μg kg(-1) minute(-1). The percentage change in MAC(BAR) was not correlated with either the log plasma ketamine or norketamine concentration. CONCLUSIONS AND CLINICAL RELEVANCE: Ketamine at clinically relevant doses of 12.5, 25, and 50 μg kg(-1) minute(-1) decreased sevoflurane MAC(BAR), although the reduction was neither dose-dependent nor linear.
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