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目的:研究辛卡利特(CCK-8)的抗吗啡作用及其作用机制。方法:采用了同步描记大鼠离体十二指肠电与机械活动的方法。结果:乙酰胆碱(ACh,300nmol/L)可使大鼠离体十二指肠峰波振幅增大、数目增多,其收缩幅度随之增大,两者呈正相关。吗啡(330nmol/L)对离体十二指肠峰波的振幅、数目和收缩幅度均无明显影响,但能选择性抑制ACh对十二指肠段电与机械活动的加强作用,呈负相关。CCK-8(0.7nmol/L)本身对十二指肠段的电与收缩活动均无明显影响,但能选择性对抗吗啡的作用,即峰波振幅、数目再次增加,收缩幅度也随之增加。在此基础上,CCK-B受体拮抗剂L-365,260(30nmol/L)能翻转CCK-8的抗吗啡作用。结论:CCK-8能对抗吗啡抑制ACh加强十二指肠活动的作用,推测该作用是通过CCK-B受体实现的。
Objective: To study the anti-morphine effect and its mechanism of acyclidine (CCK-8). Methods: Synchronous tracing of duodenal electrical and mechanical activities in rats was performed. Results: Acetylcholine (ACh, 300nmol / L) increased the amplitude of the peak amplitude of isolated rat duodenum in vitro and increased the amplitude of contractility. The positive correlation was observed between the two. Morphine (330nmol / L) had no significant effect on the amplitude, number and contractile amplitude of isolated duodenal waves, but could selectively inhibit the potentiation of ACh on the electrical and mechanical activities of the duodenum, which was negatively correlated . CCK-8 (0.7 nmol / L) itself had no significant effect on the electrical and contractile activities of the duodenum segment, but selectively antagonized the effect of morphine, ie, the peak-wave amplitude, with an increase in the number again with a corresponding increase in the amplitude of contraction . On this basis, CCK-B receptor antagonist L-365,260 (30nmol / L) can reverse the anti-morphine effect of CCK-8. CONCLUSION: CCK-8 can antagonize the effect of morphine on ACh strengthening duodenal activity, suggesting that this effect is achieved through CCK-B receptor.