甘氨酸转运体-1对芬太尼诱导的切口痛觉敏化作用

Role of glycine transporter-1 in fentanyl-induced hyperalgesia

目的：探讨甘氨酸转运体-1在芬太尼诱导的切口痛觉敏化中的作用和机制。方法：鞘内成功埋管2周后的雄性SD大鼠40只，体重为190。230g，以Brennan法制作动物切VI痛模型，并随机分为4组，NS＋NS（皮下生理盐水＋鞘内生理盐水）组、NS＋Sar（皮下生理盐水＋鞘内肌氨酸）组、Fen＋NS（皮下芬太尼＋鞘内生理盐水）组和Fen＋Sar（皮下芬太尼＋鞘内肌氨酸）组。每组各10只大鼠．通过热辐射刺激和yonFrey机械刺激进行痛行为测定，记录手术前（基础值），术后第1、2、3、4、5、6、7天大鼠的热痛和机械痛阈值，分别作统计学分析。结果：与术前基础值比较，术后第1天4组大鼠痛阈均明显降低，术后每天逐步升高。热痛和机械痛阈值以Fen＋NS组下降最为明显（P〈0．05），NS＋Sar组热痛和机械痛阈值最高，Fen＋Sar组与NS＋NS组（P〉0．05）差别不大。结论：芬太尼加重切口痛大鼠的痛觉敏化，该作用可被甘氨酸转运体-1抑制剂——肌氨酸减轻．提示甘氨酸转运体-1功能变化可能参与了芬太尼痛觉敏化作用机制。

Objective To investigate the roles of glycine transpoter-l（GlyT-1） on fentanyl-induced hyperalgesia on a rat model of incision pain and its mechanism. Methods Forty male Sprague-Dawley rats weighting 190-230 g were randomly allocated into 4 groups （n=10/group）： subcutaneous normal saline＋ intrathecal normal saline （NS＋NS） group, subcutaneous normal saline ＋ intrathecal sarcosine（NS＋Sar） group, subcutaneous fentanyl ＋intrathecal normal saline （Fen＋NS） group and subcutaneous fentanyl ＋ intrathecal sarcosine （Fen＋Sar） group. The mechanical and thermal threshold were detected with thermal radiation and von Frey filaments of rats from pre-operation to the postoperative 7th day. Results Compared with the baseline, the values of mechanical and thermal threshold in the next day of incision operation were significantly lower in all the groups. Tendency of increment of the threshold was found during the next 6 days. The decrease in thermal threshold was most extent in the Fen＋NS group. No significant difference existed between Fen＋Sar group and NS＋NS group. The mechanical and thermal thresholds were the highest in the NS＋Sar group. Conclusions Fentanyl increased hyperalgesia of incision pain in rats. This effect tends to decrease by GlyT-1 inhibitors sarcosine. It is suggested that changes of GlyT-1 function may be involved in the fentanyl induced hyperalgesia.