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机构地区:[1]北京医科大学神经科学研究中心,北京100083 [2]内蒙古包头医学院生理教研室
出 处:《中国疼痛医学杂志》1997年第4期228-232,共5页Chinese Journal of Pain Medicine
基 金:自然科学基金!39470232
摘 要:48只高针效大鼠随机分为6组,每组大鼠(8只)每天给予100Hz电针一次(30min),连续6天。其电针镇痛效果逐渐降低,形成慢性电针耐受。在第7天,6组大鼠分别皮下(S.C.)注射配药液或不同剂量的CCK-B受体桔抗剂L-365,260(0.03~3mg/kg)。S.C.注射配药液的对照大鼠仍然表现出明显的电针耐受现象,而s.c.注射L-365,260(0.1mg,0.3mg/kg)则可以有效地翻转100Hz慢性电针耐受,剂量太小(0.03mg/kg)或太大(1mg,3mg/kg)时均无效。换言之,L-365,260翻转100Hz慢性电针耐受的剂量效应曲线呈钟形曲线。上述结果表明,中枢内源性CCK参与100Hz慢性电针耐受的形成。48 rats were randomly and evenly divided into six groups. 100 Hz EA was administered for each group once a day (30 min) for 6 consecutive days. There was a gradual decrease in EA effect following repeated EA stimulation, indicating the development of chronic EA tolerance. In the seventh day, vehicle or different doses of CCK-B antagonist L-365, 260 (0. 03~3mg/ kg) was administered by subcutaneous (s. c. ) injection. Rats treated with vehicle exhibited significant tolerance to EA. In contrast, L-365, 260 at doses of 0. 1 mg, 0. 3 mg/ kg, but not 0.03 mg/ kg nor 1 or 3 mg/ kg,can effectively reverse the development of 100 Hz EA tolerance, showing a belLshaped dose response curve. These results suggest that endogenous cholecystokinin is involved in the development of chronic 100 Hz EA tolerance.
分 类 号:R338.3[医药卫生—人体生理学] R245.97[医药卫生—基础医学]
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