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Physostigmine and methylphenidate induce distinct arousal states during isoflurane general anesthesia in rats
J. Kenny, J. Chemali, J. Cotton, C. Van Dort, S. Kim, D. Ba, E. Brown, and K. Solt
Anesthesia and Analgesia, (2016)

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Although emergence from general anesthesia is clinically treated as a passive process driven by the pharmacokinetics of drug clearance, agents that hasten recovery from general anesthesia may be useful for treating delayed emergence, emergence delirium, and postoperative cognitive dysfunction. Activation of central monoaminergic neurotransmission with methylphenidate has been shown to induce reanimation (active emergence) from general anesthesia. Cholinergic neurons in the brainstem and basal forebrain are also known to promote arousal. The objective of this study was to test the hypothesis that physostigmine, a centrally acting cholinesterase inhibitor, induces reanimation from isoflurane anesthesia in adult rats.

Dextroamphetamine (but not atomoxetine) induces reanimation from general anesthesia: Implications for the roles of dopamine and norepinephrine in active emergence
J. Kenny, N. Taylor, E. Brown, and K. Solt
PLOS One, (2015)

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Methylphenidate induces reanimation (active emergence) from general anesthesia in rodents, and recent evidence suggests that dopaminergic neurotransmission is important in producing this effect. In this study, we tested the efficacy of dextroamphetamine and atomoxetine for inducing reanimation from general anesthesia in rats. Dextroamphetamine induced reanimation from general anesthesia in rodents, but atomoxetine did not induce an arousal response under the same experimental conditions. This supports the hypothesis that dopaminergic stimulation during general anesthesia produces a robust behavioral arousal response. We hypothesize that dextroamphetamine is more likely than atomoxetine to be clinically useful for restoring consciousness in anesthetized patients, mainly due to its stimulation of dopaminergic neurotransmission.

Propofol and sevoflurane induce distinct burst suppression patterns in rats
J. Kenny, M. Westover, S. Ching, E. Brown, and K. Solt
Frontiers in System Neuroscience, (2014)

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Burst suppression is an EEG pattern characterized by alternating periods of high-amplitude activity (bursts) and relatively low amplitude activity (suppressions). Burst suppression can arise from several different pathological conditions, as well as from general anesthesia. Here we review current algorithms that are used to quantify burst suppression, its various etiologies, and possible underlying mechanisms. We then review clinical applications of anesthetic-induced burst suppression. Finally, we report the results of our new study showing clear electrophysiological differences in burst suppression patterns induced by two common general anesthetics, sevoflurane and propofol. Our data suggest that the circuit mechanisms that generate burst suppression activity may differ among general anesthetics.