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1. 北京医学院生理教研室
2. 北京医学院药学系81届化学班
纸质出版日期:1984
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邱学才, 张鉴, 韩济生. 大鼠蛛网膜下腔注射dbcAMP或dbcGMP分别对抗或加强电针镇痛[J]. 针刺研究, 1984,(1):72-75.
ELECTROACUPUNCTURE ANALGESIA WAS POTENTIATED BY THE INTRATHECAL INJECTION OF dbcGMP AND ATTENUATED BY dbcAMP[J]. Acupuncture research, 1984, (1): 72-75.
近年来不少工作证明中枢神经系统中的环磷酸腺苷(cAMP)和环磷酸鸟苷(cGMP)在针刺镇痛中起着重要作用。例如大鼠侧脑室注射cAMP可明显拮抗电针镇痛和吗啡镇痛
射注cGMP可加强电针镇痛和吗啡镇痛。如果将微量的cGMP或其衍生物二丁酰cGMP(dbcGMP)注入大鼠缰核内
不但加强电针镇痛
并可延缓电针耐受的发展。但两种环核苷酸在脊髓中对针刺镇痛起何种作用
目前尚未见报道。本工作将二丁酰cAMP(dbcAMP)或二丁酰cGMP注入大鼠脊髓蛛网膜下腔内
观察其对电针镇痛的影响。
We have shown that the effect of acupuncture analgesia (AA) and mo- rphine analgesia could be dose-dependently attenuated by intracerebrove- ntricular (icv) injection of cAMP
and potentiated by cGMP. In the present study dibutyryl derivatives of cAMP or cGMP were injected into the subara- chnoid space of the spinal cord to see their effects on AA. Intrathecal catheterization was performed under ether anesthesia. polye- thylene tube of 0.61 mm o. d. was introduced through foramen magnum into the subarachnoid space
reaching the level of thoracolumbar junction. Measurement of tail-flick latency started 4 h after surgery. No significant fluctuation of tail-flick latency was noticed in a period of 60 min follo- wing the intrathecal administration of 50 μg/10 μl of dbcAMP
20μg/10 μl of dbcGMP or 10μl of artificial CSF. In electroacupuncture (EA) experiments
rats were given intrathecal injection of CSF
followed 15 min later by a session of EA at Zusanli and Sanyinjiao points (2~15 Hz
with increasing voltage from 1V to 2.5V in 30 min). Tail-flick latency was assessed every 10min. The percentage increases of latency in the 3 measurements during the EA period were ave- raged as the average EA analgesia. One hour later
the EA experiment was repeated with intrathecal injection of dbcAMP instead of CSF. The differe- nce in average EA aualgesia between dbcAMP and CSF sessions in individual animals was taken for statistical analysis. It was shown that EA effect was decreased by 30±7%
58±12% and 75±12% in groups of rats injected with 12.5
25 and 50μg of dbcAMP respectively (P<0.01 in each group
n=7~11). On the contrary
an augmentation of AA by 13±7% (p>0.05)
25±10% (p<0.05) and 29±10%±(p<0.05) was observed in groups of rats injected with 10
20 and 40μg of dbcGMP (n=10~13). The results indicate a marked attenuation of AA by intrathecal injection of dbcAMP and a mo- derate potentiation of AA by dbcGMP. A similar effect on AA was thus shown for cyclic nucleotides both in the brain and in the spinal level.
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