【作者】 李静；

【导师】 陆杰；

【作者基本信息】 重庆医科大学 ， 生理学， 2009， 硕士

【摘要】 目的:探讨胃动素对膈下迷走神经传入自发放电和扩胃诱发放电的影响及其相应的机制。方法:实验在SD大鼠身上进行,记录膈下迷走神经传入自发和扩胃诱发的放电变化,静脉注射不同剂量胃动素,以及先用5-HT3受体阻断剂昂丹司琼或M受体阻断剂阿托品处理,再给胃动素观察其放电变化。结果:小剂量胃动素(1μg/kg)自发和诱发均无无显著变化;中剂量(5μg/kg)和大剂量(40μg/kg)胃动素注射后,自发放电和诱发放电均显著增加;昂丹司琼能够完全阻断大剂量的作用(P<0.05);阿托品对大剂量胃动素的作用有一定改变,但无统计学意义(P>0.05)。昂丹司琼能够单独阻断迷走传入神经放电(P<0.05),阿托品对迷走传入放电有抑制作用,但无统计学意义。结论:胃动素引起迷走传入自发和诱发放电增加,迷走传入神经参与了胃动素对胃肠感觉影响后的信息传递,而5-HT3受体也可能参与这种传递过程。目的:观察静脉注射阿奇霉素对大鼠胃内压和胃电慢波的影响,并探讨阿奇霉素作用所依赖的神经和受体。方法:实验在48只乌拉坦麻醉的成年SD大鼠上进行。颈静脉注射不同剂量的阿奇霉素或生理盐水(1ml),观察胃内压和胃电慢波变化(30只);先注射阿托品,再注射大剂量阿奇霉素观察胃内压变化(6只);膈下迷走神经切断后,注射大剂量阿奇霉素观察胃内压和胃电变化(12只)。结果:静脉注射中剂量(75mg/kg)和大剂量(150mg/kg)阿奇霉素后,大鼠胃内压增加;两种剂量对胃慢波电位幅度和频率均无明显影响。使用阿托品后,阿奇霉素对胃内压的影响几乎完全阻断。膈下迷走神经切断后,阿奇霉素对胃内压作用被反转,胃内压下降明显,而胃电无明显变化。结论:静脉注射阿奇霉素可增加胃内压,该效应可能通过迷走神经和胆碱能受体完成,阿奇霉素对胃电慢波幅度和频率未见明显作用。更多还原

【Abstract】 Objectives: To investigate the effect of motilin on spontaneous afferent nerve discharge and gastric distention-induced afferent nerve discharge and explore the corresponding mechanism.Methords: Experiments were performed in anesthetized SD rats. The sensory impulses of subdiaphragmatic vagal nerve were recorded by the RECORDER. Different dosages of motilin were intravenous injection. Some rats were pretreated with ondansetron or atropine, and then injected high-dose motilin.Results: Intravenous low dose (1μg/kg) had no effect, intravenous medium dose and high dose (5μg/kg and 40μg/kg respectively) caused obvious increase of spontaneous afferent discharge and gastric distention-induced afferent discharge. Pretreatment with ondansetron almost completely blocked the effects of motilin. Atropine had no obvious influence with the effect of high-dose motilin. Ondansetron inhibited afferent nerve discharge by itself,and atropine also did, but the latter failed to reach statistical significance.Conclusion: Motilin can excite spontaneous afferent nerve discharge and gastric distention-induced afferent nerve discharge. Vagal afferent nerve may play roles in the actions of motilin, 5-HT receptor are probably involved in the effect, but not atropine . Objective: To observe the effect of azithromycin on intragastric pressure(IGP) and gastric electrical slow wave, and explore the dependent nerve and receptor.Methords: Experiments were performed in anesthetized SD rats. Animals received intravenous injection of different doses azithromycin or normal saline(1 ml), both IGP and gastric electrical activity were recorded by BL-410 Biological signal recording system(n=30). Pretreatment of atropine was intraperitoneal injection, and then injected high-dose azithromycin and recorded IGP(n=6). Pretreatment of vagotomy was carried out, and then used normal saline or high-dose and recorded IGP and gastric electrical activity(n=12).Results: Intravenous medium dose azithromycin(75mg/kg) and high dose azithromycin(150mg/kg) caused the increase of IGP, Different doses had no obvious influence on gastric electrical slow wave amplitude and frequency. No obvious changes in both IGP and gastric electrical activity was observed in normal saline. Atropine almost completely blocked the effect of azithromycin on IGP. Pretreatment of subdiaphragmal vagotomy turned the increase of IGP induced by azithromycin, IGP discreased obviously ,but gastric electrical activity were not changed.Conclusion: Intravenous azithromycin could make IGP increase, this effect might rely on vagus and cholinergic receptor; Azithromycin might have no obvious effect on gastric electrical slow wave amplitude and frequency.更多还原