Browsing by keyword "dexmedetomidine"
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D-Amphetamine Rapidly Reverses Dexmedetomidine-Induced Unconsciousness in RatsD-amphetamine induces emergence from sevoflurane and propofol anesthesia in rats. Dexmedetomidine is an alpha2-adrenoreceptor agonist that is commonly used for procedural sedation, whereas ketamine is an anesthetic that acts primarily by inhibiting NMDA-type glutamate receptors. These drugs have different molecular mechanisms of action from propofol and volatile anesthetics that enhance inhibitory neurotransmission mediated by GABAA receptors. In this study, we tested the hypothesis that d-amphetamine accelerates recovery of consciousness after dexmedetomidine and ketamine. Sixteen rats (Eight males, eight females) were used in a randomized, blinded, crossover experimental design and all drugs were administered intravenously. Six additional rats with pre-implanted electrodes in the prefrontal cortex (PFC) were used to analyze changes in neurophysiology. After dexmedetomidine, d-amphetamine dramatically decreased mean time to emergence compared to saline (saline:112.8 +/- 37.2 min; d-amphetamine:1.8 +/- 0.6 min, p < 0.0001). This arousal effect was abolished by pre-administration of the D1/D5 dopamine receptor antagonist, SCH-23390. After ketamine, d-amphetamine did not significantly accelerate time to emergence compared to saline (saline:19.7 +/- 18.0 min; d-amphetamine:20.3 +/- 16.5 min, p = 1.00). Prefrontal cortex local field potential recordings revealed that d-amphetamine broadly decreased spectral power at frequencies < 25 Hz and restored an awake-like pattern after dexmedetomidine. However, d-amphetamine did not produce significant spectral changes after ketamine. The duration of unconsciousness was significantly longer in females for both dexmedetomidine and ketamine. In conclusion, d-amphetamine rapidly restores consciousness following dexmedetomidine, but not ketamine. Dexmedetomidine reversal by d-amphetamine is inhibited by SCH-23390, suggesting that the arousal effect is mediated by D1 and/or D5 receptors. These findings suggest that d-amphetamine may be clinically useful as a reversal agent for dexmedetomidine.
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Evaluation of the impact of a prescribing guideline on the use of intraoperative dexmedetomidine at a tertiary academic medical centerObjective: To evaluate usage patterns of dexmedetomidine in the operating room after implementation of a prescribing guideline. Methods: We conducted a retrospective analysis to evaluate the impact of a prescribing guideline on usage patterns of dexmedetomidine in the operating room at a tertiary, academic medical center during one-month period pre- (July 2010) and post-guideline (July 2011 and July 2012) implementation. Results: A total of 267 patients received intraoperative dexmedetomidine during the study period. Dexmedetomidine use in surgical procedures decreased post-guideline implementation [5.7% (pre) vs. 1.9% and 3.3% (post)]. The most common guideline-based indication for intraoperative dexmedetomidine was for anesthesia during bariatric surgery (41% and 38% in 2011 and 2012, respectively). We estimated a cost-avoidance of $308,856 over the two-year period after guideline implementation. Conclusion: Our results suggest that implementation of a prescribing guideline for the use of dexmedetomidine in the operating room is feasible and associated with improved utilization patterns.

