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Pharm Res. 1985 May;2(3):137-9. doi: 10.1023/A:1016367417686.
Possible central cholinergic modulation of acute peripheral inflammation was investigated in rats, adopting the carrageenin-induced acute pedal edema as the experimental model. Intracerebroventricularly (icv) administered acetylcholine (Ach) and tremorine, a central cholinomimetic agent, significantly augmented the inflammation, whereas hemicholinium, which inhibits Ach synthesis, attenuated the edema. Paradoxically, icv administered atropine sulphate induced an Ach like pro-inflammatory effect and also failed to affect the Ach action. The atropine-induced inflammation promoting effect was annulled after hemicholinium pre-treatment, suggesting that it was dependent on the integrity of central cholinergic function. The pro-inflammatory effect of icv Ach was negated after peripheral administration of atropine ethoiodide. It is suggested that the carrageenin inflammation promoting effect of centrally administered Ach is due to enhanced peripheral cholinergic activity.
研究人员采用角叉菜胶诱导的急性足跖肿胀作为实验模型,探讨了中枢胆碱能系统对急性外周炎症的可能调节作用。结果表明,脑室内给予乙酰胆碱(Ach)和震颤素(一种中枢拟胆碱药)可显著增强炎症反应,而抑制 Ach 合成的 hemicholinium 则可减轻水肿。矛盾的是,脑室内给予硫酸阿托品可诱导类似于 Ach 的促炎作用,并且也未能影响 Ach 的作用。hemicholinium 预处理后可消除阿托品诱导的促炎作用,提示其依赖于中枢胆碱能功能的完整性。外周给予硫酸阿托品乙碘化物后,脑室内 Ach 的促炎作用被否定。这表明中枢给予 Ach 对角叉菜胶炎症的促进作用是由于增强了外周胆碱能活性。