Devazepide reversed effect of sincalide against morphine on rat jejunal activities.

M Y Xu, X P Yang, H B Jin, C X Yang, L Z Yang
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Abstract

Aim: To study the antagonism of sincalide to the effect of morphine and its mechanism.

Methods: The electrophysiologic and mechanic activities of rat jejunum in vitro were recorded.

Results: Acetylcholine (ACh, 150 nmol.L-1) increased the spike potential amplitude (SPA) and the number (SPN) of rat jejunum in vitro, followed by an increase of jejunal contraction amplitudes (CA), showing a positive correlation. Morphine 330 nmol.L-1 inhibited the potentiation of ACh, showing a negative correlation. Sincalide 0.7 nmol.L-1 antagonized the effects of morphine, i.e., the SPA and SPN were increased again, followed by an increase of CA. CCK-A receptor antagonist devazepide (10 nmol.L-1) reversed the antagonism of sincalide to the effect of morphine.

Conclusion: Sincalide antagonized the effect of morphine which inhibited the potentiation of ACh on jejunal activities in vitro. The antagonistic effect of sincalide on morphine was mainly mediated by CCK-A receptor.

地伐赛得逆转辛卡啶对吗啡对大鼠空肠活动影响。
目的:研究辛卡苷对吗啡作用的拮抗作用及其机制。方法:记录大鼠离体空肠的电生理和力学活动。结果:乙酰胆碱(ACh, 150 nmol.L-1)使离体大鼠空肠的尖峰电位振幅(SPA)和数量(SPN)增加,随后使空肠收缩振幅(CA)增加,两者呈正相关关系。吗啡330 nmol。L-1抑制乙酰胆碱的增强,呈负相关。0.7 nmol。L-1可拮抗吗啡的作用,即SPA、SPN再次升高,CA随之升高。CCK-A受体拮抗剂地伐匹德(10 nmol.L-1)可逆转辛卡啶对吗啡的拮抗作用。结论:辛卡啶能拮抗吗啡对乙酰胆碱增强空肠活性的作用。辛卡苷对吗啡的拮抗作用主要由CCK-A受体介导。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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