【摘要】 目的和方法：本工作旨在研究免迷走复合区（ＤＶＣ）内ＴＲＨ对奥迪氏括约肌（ＳＯ）肌电的调节作用及外周途径。结果：（１）ＤＶＣ内注射ＴＲＨ（０．８ｎｍｏｌ，１μｌ）后，慢波电位（ＳＷ）频率不变，但锋电位频率（ＦＳＰＳＯ）及幅度（ＡＳＰＳＯ）、锋电位发生率（ＩＳＰ）明显增加．（２）ＤＶＣ内分别注射不同剂量ＴＲＨ（０．１３，０．２５，０．５０，０．８０，１．３０ｎｍｏｌ，１μｌ）后，各剂量ＴＲＨ均能引起ＦＳＰＳＯ增加。随注射剂量的增加，ＳＯ反应强度和持续时间均增加，呈现明显的剂量反应关系。（３）ＤＶＣ内注射ＴＲＨ兴奋ＦＳＰＳＯ的效应可被静脉注射阿托品（０．２ｍｇ／ｋｇ）或迷走神经切断完全阻断，但不能被静脉注射酚妥拉明（１．５ｍｇ／ｋｇ）、心得安（１．５ｍｇ／ｋｇ）或脊髓切断术所阻断。结论：ＤＶＣ内ＴＲＨ可能对ＳＯ肌电有重要的调节作用，这种作用是通过迷走神经及外周Ｍ受体介导。更多还原

【Abstract】 Aim and Methods: This study was performed to investigate the effects of TRH in DVC on motility of the sphincter of Oddi(SO). After fasting about 15 18 hr, the rabbits are anesthetized with urethane (1.0 g/kg) , the myoelectric signals of SO were induced by a pair of copper electrodes inserted into subsera. Results:1. Microinjection of TRH (0.8 nmol,1μl) into DVC raised frequency of spike potentials of SO (FSPSO), amplitude of spike potentials of SO (ASPSO) and incidence of spike potentials (ISP), but the frequency of slow wave did not change. 2. All the doses of TRH (0.13、0.25、0.50、0. 80、1.30 nmol,1μl) injected into DVC could increase the FSPSO. As the dose of TRH was increasing, the reaction and the duration of the reaction were also increasing. 3. The effects of TRH in DVC on FSPSO could be completely abolished by atropine (0.2 mg/kg, iv.) or vagotomy, but could not inhibited by phentolamine (1.5 mg/kg, iv.), propranolol(1.5 mg/kg, iv) or transecting the spinal cord through T1. Conclusion:Via vagus nerve and peripheral M receptors, thyrotropin releasing hormone in DVC may play an important role in regulating the motility of SO.更多还原