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脑内钙和镁对抗吗啡镇痛和电针镇痛
引用本文:周仲福,宣雨霆,韩济生.脑内钙和镁对抗吗啡镇痛和电针镇痛[J].针刺研究,1983(4).
作者姓名:周仲福  宣雨霆  韩济生
作者单位:北京医学院生理教研室,北京医学院生理教研室,北京医学院生理教研室
摘    要:<正> 已知一些单价和两价金属离子对于神经系统的正常活动具有重要意义。特别是钙离子(Ca~(++))对于神经膜的稳定性和通透性、神经冲动的传导、神经末梢递质的释放、递质作用于突后触膜引起的生物效应、以及对第二信使的生成和作用等等,都起着关键的作用。许多资料表明,吗啡类药和内源性吗啡样物质(内啡素)的镇痛作用可能就是通过降低中枢某些部位Ca~(++)的功能而实现的。至于镁(Mg~(++))是否与Ca~(++)有类似的作用,文献资料很不一致,有待进一步清澄。


ANTAGONISTIC EFFECT OF CEREBRAL CALCIUM AND MAGNESIUM ON MORPHINE ANALGESIA AND ELECTROACPUNCTURE ANALGESIA
Abstract:In rabbits provided with chronic intracerehroventricular cannula, CaCl_2 or MgC1_2 was injected intraventricularly (ivt) to increase the cerebral content of Ca~(++) and Mg~(++), and CDTA, the cation chelator, was injected ivt to lower the cerebral content of cations including Ca~(++) and Mg~(++) to see its effect on the analgesia induced by electroacupuncture (EA) or by morphine. 1. The effect on EA analgesia: EA of 2-15Hz, 1v, 10 min was given to hind leg points Zusanli and Qunlun, 10 rain after the ivt injection of one of the following chemicals: CaCl_2, MgCl_2 or CDTA in a dose of 0.5 μmol, or 50μl of normal saline as control. Nociception was tested by the latency of the head jerk induced by radiant heat applied on the skin over the snout. It was shown that EA analgesia found in CaCl_2 group(28±8%) was much lower than that of the saline control group(133±13%,p<0.001). A decrease in EA analgesia was also observed in rabbits injected with MgCl_2 (47±11% vs 123±15%, p<0.001). Ivt injection of the chelator CDTA, on the contrary, resulted in a potentiation of EA analgesia(CDTA group 164±15% vs saline group 104±19%, p<0.05). No significant chan- ges in pain threshold were seen when these chemicals were injected alone. The results indicate that Ca~(++) and Mg~(++) in brain may exert an antagonis- tic effect on EA analgesia 2. The effect on morphine analgesia: Groups of rabbits were given ivt injection of one of the following chemicals: CaCl_2 4 μmol, MgCl_2 2 μmol, CDTA 1.4 μmol, or normal saline 50 μl, followed 10 min later by iv injection of morphine(3 or 6 mg/kg). Pain threshold changes were monitored for 1 h. A decrease in morphine analgesia was shown both in CaCl_2 group(50±26% vs 197±2%, p<0.001) and in MgCl_2 group (54±11% vs 145±19%, p<0.001). Ivt injection of CDTA, however, caused a marked potentiation of morphine analgesia (166+20% as compared with 105±10% in control group, p<0.05). An antagonistic effect of cerebral Ca~(++) and Mg~(++) was thus shown also on morphine analgesia. That both EA and morphine analgesia were attenuated by an increase in cerebral Ca~(++) and Mg~(++) and augmented by a decrease in brain cations implies a similarity in the mechanisms of action for these two analgesic processes.
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