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本工作研究了中枢阿片肽系统在手术创伤介导大鼠免疫功能低下效应中的作用以及电针对创伤介导的免疫功能低下效应的影响。在手术创伤大鼠模型上以自然杀伤细胞活性（NKactivity）、刀豆蛋白A诱导的脾淋巴细胞转化率和白介素-2（IL-2）诱生水平为指标，观察侧脑室注射（icv）阿片受体拮抗剂纳洛酮（naloxone）及电针穴位的作用。结果表明，创伤后大鼠的NK活性、脾淋巴细胞转化率和IL-2诱生水平均明显低于创伤前（P＜0．001，P＜0．05和P＜0．001）。纳洛酮（20μg,icv）明显地拮抗由创伤导致的NK活性和IL-2诱生水平抑制状态。电针足三里（St36），阑尾穴（Extra33）后明显改善创伤引起的NK活性、脾淋巴细胞转化率和IL-2诱生水平的抑制。提示中枢内阿片肽系统参与创伤应激介导的免疫功能低下，而电针具有调整创伤应激介导的免疫机能低下效应的作用。
This work investigated the role of the central opioid system in the surgical trauma-mediated immunodeficiency in rats and the effects of electroacupuncture on wound-mediated immune dysfunction. The intracerebroventricular (icv) opioid injection was performed on the model of traumatic injury on the basis of NKactivity, concanavalin A induced spleen lymphocyte transformation and interleukin-2 (IL-2) Receptor antagonist naloxone and electroacupuncture points. The results showed that the activity of NK, the rate of spleen lymphocyte transformation and the level of IL-2 induced in traumatized rats were significantly lower than those before trauma (P <0.001, P <0.05 and P <0.001). Naloxone (20 μg, icv) significantly antagonized wound-induced NK activity and IL-2 induced-level inhibition. Electroacupuncture at Zusanli (St36) and Extra33 significantly inhibited the wound-induced NK activity, the splenic lymphocyte transformation rate and the IL-2 induced level. Suggesting that the central opioid system is involved in traumatic stress-mediated immune dysfunction, while electroacupuncture has the effect of modulating traumatic stress-mediated immunodeficiency.