脑内不少神经递质以环磷酸腺苷(cA-MP)和环磷酸鸟苷(cGMP)作为第二信使

“调节着细胞功能。近年来

对cGMP在中枢镇痛中的作用引起了人们的重视。我们以前的工作证明

脑室内注射cGMP可使痛阈明显提高

并能增强大鼠电针镇痛效应。初步观察到

这可能与乙酰胆碱(Ach)和阿片样物质(OLS)的作用机理有关。有资料证明

Ach、OLS与脑内cGMP有着密切的关系

并设想cGMP可能是传递阿片受体兴奋的细胞内介质。本工作观察了脑室注射cGMP对It was observed in our previous experiments that intraventricular in- jection of cGMP elevated pain thresholds and potentiated the effect of acupuncture analgesia(AA). In this study we are to observe the effect of naloxone and atropine on analgesic action by cGMP. Female rats weighing 180-280g were used. Pain threshold wasassesssed by the tail flick test. "Zusanli" and "Sanyinjiao" were bilaterally stimula- ted with electroacupuncture for 30 rain. The percentage of the mean of three pain thresholds in a trial was taken as the index of AA. 1. Intraventricular injection of cGMP(400μg) led to a marked increase of pain threshold by 57%-90%

which recovered within 80-100 min after injection. When cGMP was used in combination with naloxone (30μg)

the pain threshold was only slightly increased (+8%

2

6%). The diffe- rence between these two groups was significant(P

<

0.05); but as com- pared with the saline group

no significant difference (P

>

0.20)was obs- erved. The results indicated that the analgesic effect of cGMP could be reversed by naloxone. 2. cGMP markedly potentiated the effect of AA. These values were 242% as great as that of the control. When cGMP was used in combina- tion with naloxone

the effect of AA was decreased by 99% (P

<

0.001)

the value being 143% of the control. The effect of AA was very similar to that of naloxone group alone (P

>

0.20). The results suggested that naloxone could antagonize the effect of AA strengthened by cGMP. 3. Atropine(5mg/kg

i.p.)did not significantly affect the pain thre- shold and the effect of AA. As compared with the saline group

no signi- ficant difference(P

>

0.10 and P

>

0.50

respectively) was observed. But the enhancing effect of cGMP on pain threshold and AA could be rever- sed by atropine. The evidence mentioned above suggests that the enhancing action of cGMP on AA could be reversed by blocking of opiate receptor with nalo- xone or blocking of muscarinic receptor of ACh with atropine.