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N-甲基-D-天冬氨酸受体在瑞芬太尼诱发痛觉过敏中作用的研究进展 被引量:5

Research progress on the role of N-methyl-D-aspartate receptors in remifentanil-induced hyperalgesia
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摘要 背景瑞芬太尼作为较理想的超短效阿片类镇痛药被广泛用于临床麻醉中。随着对其研究的深入,其所诱发的术后痛觉过敏引起了人们关注。最近国内外对瑞芬太尼诱发术后痛觉过敏的机制进行大量研究,研究最为深入的是脊髓背角N-甲基-D-天冬氨酸(N-methyl-D-aspartate,NMDA)受体。目的通过对近年NMDA受体在瑞芬太尼诱发术后痛觉过敏中所起作用的研究进行回顾和总结,帮助读者了解国内外相关研究的最新趋势和进展。内容就痛觉过敏定义、NMDA受体的信号转导机制及其在瑞芬太尼诱发痛觉过敏中作用的研究进展进行综述,阐明NMDA受体系统在瑞芬太尼诱发的痛觉过敏中起着关键作用。趋向深入研究NMDA受体在痛觉过敏中的作用机制,将NMDA受体作为分子治疗靶点,可为临床上痛觉过敏的预防提供广阔的思路和前景。 Background Remifentanil as an ideal ultra-short opioid is widely used in clinical anesthesia. With the deepening research on it, remifentanil-indueed postoperative hyperalgesia has attracted more attention. Recently, there has been a lot of studies exploring the mechanisms of remifentanil-induced hyperalgesia at home and abroad. The profound studies are about the N- methyl-D-aspartate (NMDA) receptors in dorsalhorn neurons. Objective The relevant literatures involved in the role of N-methyl- D-aspartate receptors in remifentanil-induced postoperative hyperalgesia in recent years were summarized, which help readership to update the latest information about this topic. Content This review provides a comprehensive summary of the definition of hyperalgesia and the signal transduction mechanism of NMDA receptor as well as its progressions in remifentanil-induced hyperalgesia. Those researches suggest that the activation of NMDA receptors play a critical role in the development of opioid-induced hyperalgesia. Trend The mechanism of remifentanil-induced postoperative hyperalgesia is complex, fully understanding the effects of NMDA receptors on remifentanil-induced hyperalgesia will provide a wide strategy and prosperity for preventing clinical hyperalgesia.
出处 《国际麻醉学与复苏杂志》 CAS 2015年第3期271-274,共4页 International Journal of Anesthesiology and Resuscitation
关键词 瑞芬太尼 痛觉过敏 N-甲基-D-天冬氨酸受体 NR2B亚单位 糖原合成酶激酶-3Β γ-氨基丁酸能去抑制 Remifentanil Hyperalgesia N -methyl-D-aspartate receptor NR2B subunit Glycogen synthase kinase-3β Gamma-aminobutyric acid ergic disinhibition
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