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目的探讨无痛注射选择性5-羟色胺再吸收抑制剂(SSRI)与盐酸利多卡因缓解新生大鼠疼痛时疼痛部位5-羟色胺1A(5-HTIA)的表达及同期脑啡肽的表达。方法将14日龄新生SD大鼠随机分为对照组、盐酸氟西汀(SSRI)组、盐酸利多卡因组,每组10只。用血糖针针尖完全刺入新生SD大鼠臀部作为疼痛刺激,针刺后立即用injex无针注射笔在针刺部位分别注射9 g·L-1盐水、SSRI药液及盐酸利多卡因药液,处死大鼠,取其臀部皮肤组织进行石蜡包埋,免疫组织化学法检测其局部5-HTIA分布部位,通过图像分析系统分析5-HTIA水平,同时取其全脑匀浆,离心后用酶联免疫吸附法检测其脑啡肽水平。结果疼痛刺激试验完成前各实验组均无5-HTIA阳性颗粒表达;试验后各实验组皮肤组织表皮质均有5-HTIA阳性颗粒表达;SSRI组5-HTIA阳性反应区明显大于对照组和盐酸利多卡因组。免疫组织化学法检测显示5-HTIA在SSRI组为0.241 5±0.020 5,显著高于对照组(0.204 9±0.016 4)(P<0.01),也显著高于盐酸利多卡因组(0.168 1±0.022 1)(P<0.01)。SSRI组新生大鼠全脑匀浆脑啡肽(39.706±2.864)ng·L-1,明显高于对照组[(36.627±2.151)ng·L-1](P<0.05);盐酸利多卡因组为(39.087±3.577)ng·L-1,也明显高于对照组(P<0.05);SSRI组和利多卡因组脑啡肽表达比较无差异。结论无痛注射SSRI缓解疼痛的机制可能是通过抑制皮肤神经接头处5-HTIA的再吸收而抑制疼痛的神经传导。无痛注射SSRI和盐酸利多卡因最终均是通过增加脑啡肽而发挥镇痛作用。
Objective To investigate the effect of painless injection of selective serotonin reuptake inhibitors (SSRI) and lidocaine hydrochloride on 5-HTIA and enkephalin expression in pain in neonatal rats. Methods 14-day-old neonatal SD rats were randomly divided into control group, fluoxetine hydrochloride (SSRI) group and lidocaine hydrochloride group, 10 rats in each group. Using the needle of the blood glucose needle to completely penetrate the buttocks of the newborn SD rats as a pain stimulus, immediately inject the injex needle-free injection pen with 9 g · L-1 saline, SSRI solution and lidocaine hydrochloride solution , The rats were sacrificed, and the buttocks skin tissues were paraffin-embedded. The local 5-HTIA distribution sites were detected by immunohistochemistry. The 5-HTIA levels were analyzed by image analysis system. Meanwhile, The levels of enkephalins were detected by the method of immunosorbent assay. Results No 5-HTIA positive particles were found in all the experimental groups before the pain stimulation test was completed. 5-HTIA positive particles were expressed in the epidermis of skin tissue in each experimental group after the stimulation test. The positive reaction zone of 5-HTIA in SSRI group was significantly larger than that of the control group and hydrochloric acid Lidocaine group. Immunohistochemistry showed that the 5-HTIA in SSRI group was 0.241 5 ± 0.020 5, significantly higher than that in control group (0.204 9 ± 0.016 4) (P <0.01) and significantly higher than that in lidocaine hydrochloride group (0.168 1 ± 0.022 1) (P <0.01). The total enkephalin (39.706 ± 2.864) ng · L-1 in whole brain homogenate of SSRI group was significantly higher than that of the control group [(36.627 ± 2.151) ng · L -1] (P <0.05) Group (39.087 ± 3.577) ng · L-1, which was also significantly higher than that of the control group (P <0.05). There was no difference in enkephalin expression between the SSRI group and the lidocaine group. Conclusions The mechanism of painless SSRI pain relief may be to inhibit the painful nerve conduction by inhibiting the reabsorption of 5-HTIA at the nerve junction of the skin. Painless injection of SSRI and lidocaine hydrochloride eventually exert an analgesic effect by increasing enkephalin.