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目的 :观察静脉注射α 肾上腺素能受体激动剂和拮抗剂以及刺激交感神经 (sympatheticstimulation ,SS)对糖尿病痛过敏大鼠尾神经中C和Aδ单位的影响。 方法 :测定糖尿病过敏大鼠尾神经C和Aδ单位放电情况及相关因素对其影响。结果 :在注射α2 受体激动剂可乐定后 ,糖尿病痛过敏大鼠无自发放电的部分C(3 16 )和Aδ(14 35 )单位由静息状态转入活动状态 ;在具有自发放电的C(8 4 1)和Aδ(2 2 79)单位中 ,α2 受体拮抗剂育亨宾能阻断这些单位的自发电活动 ,而可乐定则使这些单位的放电频率增加 ;α1 受体激动剂苯肾上腺素和拮抗剂哌唑嗪不影响C和Aδ单位的电活动。SS可引起糖尿病痛过敏大鼠无自发放电的部分C(10 33)和Aδ(2 6 5 7)单位产生新的传入活动 ,而注射育亨宾后SS不再对这些单位产生兴奋作用 ;哌唑嗪和β 受体拮抗剂心得安不影响SS对C和Aδ单位的作用 ;SS能引起糖尿病痛过敏大鼠有自发放电的C(8 4 1)和Aδ(2 2 79)单位的放电频率增加 ,注射育亨宾后这些单位的自发电活动消失 ,重复SS不再使这些单位产生传入放电 ;而哌唑嗪则无此作用。 结论 :去甲肾上腺素(NA)通过α2 肾上腺素能受体兴奋糖尿病痛过敏大鼠的C和Aδ单位。
OBJECTIVE: To observe the effects of α adrenergic receptor agonists and antagonists and sympathetic stimulation (SS) on the C and Aδ units in the caudal nerve of rats with diabetic hyperalgesia. Methods: The discharge of C and Aδ units in the tail nerve of diabetic rats with allergic reaction and the related factors were determined. RESULTS: After injection of clonidine, an agonist of α2 receptor, part of C (3 16) and Aδ (14 35) without spontaneous discharge in diabetic hyperalgesia rats were switched from resting state to active state; in spontaneous discharge C (8 4 1) and Aδ (2 2 79) units, the α2-receptor antagonist yohimbe blocked the spontaneous electrical activity of these units while clonidine increased the discharge frequency of these units; the α1 -receptor agonist Phenylephrine and the antagonist prazosin did not affect the electrical activity of C and Aδ units. SS caused new spontaneous afferent activities in some C (1033) and Aδ (2657) units without spontaneous discharge in rats with allergic hyperesthesia, whereas SS was no longer stimulated by these units after injection of yohimbine; Prazosin and beta-receptor antagonist propranolol did not affect the effect of SS on C and Aδ units; SS induced a spontaneous discharge of C (8 4 1) and Aδ (2 2 79) units in diabetic hyperalgesic rats The frequency increased, spontaneous activity disappeared in these units after injection of yohimbine, repeated SS no longer caused these units to have an in-discharge; whereas prazosin did not. CONCLUSION: Norepinephrine (NA) is stimulated by α2 adrenergic receptors in C and Aδ units of allergic rats with diabetic pain.