右美托咪定增强笑气镇痛作用:作用机制。

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道森C，马D，周A，梅兹M

右美托咪定增强笑气镇痛作用:作用机制。

麻醉学杂志2004年4月;100(4):894-904。

PubMed ID

15087625 (PubMed视图

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摘要

背景:一氧化二氮和右美托咪定被认为分别通过脊髓内的α 2B和α 2a肾上腺素能受体亚型介导镇痛(在非交流生物中抗镇痛)。一氧化二氮和右美托咪定对蓝斑内的神经元活动产生截然相反的影响，蓝斑是调节镇痛的关键部位。由于这些差异，作者探讨了两种镇痛药联合使用是否能提供令人满意的镇痛效果。方法:采用大鼠甩尾潜伏期试验评价氧化亚氮和右美托咪定腹腔和鞘内给药的镇痛效果。为了研究相互作用，大鼠在接触一氧化二氮之前立即用右美托咪定腹腔内或鞘内预处理，使每种药物的抗伤害作用峰值重合。为了评估对耐受性的影响，右美托咪定在对氧化亚氮耐受性发展时给予。c-Fos的表达被用来评估蓝斑的神经元活动。结果:氧化亚氮和右美托咪定增加尾弹潜伏期，氧化亚氮的ED50(平均+/- SEM)为55.0 +/- 2.2% atm，微克/kg腹腔注射右美托咪定为27.6 +/- 5.1，鞘内注射右美托咪定为2.9 +/- 0.1微克。系统给药右美托咪定和一氧化二氮的组合产生了加性镇痛相互作用;然而，神经轴给药右美托咪定与笑气有协同作用。 Tolerance to nitrous oxide was reversed by coadministration of dexmedetomidine. Prazosin, the alpha 1-/alpha 2B-adrenoceptor antagonist, attenuated the analgesic effect of nitrous oxide and prevented dexmedetomidine-induced reversal of tolerance to nitrous oxide. Nitrous oxide-induced increase of neuronal activity in the locus ceruleus was reversed by dexmedetomidine. CONCLUSION: The synergistic analgesic interaction between nitrous oxide and dexmedetomidine within the spinal cord is obscured by a supraspinal antagonism when dexmedetomidine is administered systemically in the pretolerant state. After tolerance to nitrous oxide develops, supraspinal functional antagonism no longer obtains exposing the synergistic action at the level of the spinal cord, which expresses itself as a reversal of the tolerant state. The authors speculate that the addition of dexmedetomidine to nitrous oxide is likely to provide enhanced and more durable analgesia in settings in which nitrous oxide is currently used alone (e.g., labor and dental surgery).

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药物靶点

药物	目标	种类	生物	药理作用	行动
Dexmedetomidine	α - 2a肾上腺素能受体	蛋白质	人类	是的	受体激动剂	细节