大鼠DMV注射AVP对胃运动和胃酸分泌的影响及其机制的研究

发布时间：2018-02-21 10:35

本文关键词： 大鼠迷走神经背核精氨酸加压素胃运动胃酸分泌　出处：《山东师范大学》2011年硕士论文　论文类型：学位论文

【摘要】：大鼠束缚-浸水应激(restraint water-immersion stress, RWIS)条件下,胃运动和胃酸分泌机能均发生紊乱。其中在调控胃肠功能的较高级中枢下丘脑前部,视上核(SON)、室旁核(PVN)神经元活动最强烈,在初级中枢延髓,迷走神经背核(DMV)神经元活动最强烈,这些结果提示,可能有SON→DMV→胃的神经调控环路的存在。若有,其神经递质及其受体是什么,至今尚不明确。已知SON、PVN主要由精氨酸加压素(AVP)能和催产素(OT)能神经元组成,已有文献报道:OT能神经元有纤维末梢止于DMV;向DMV注射OT可抑制胃运动,刺激胃酸分泌,说明OT可通过DMV对胃机能进行调控,那么,AVP能神经元是否存在于DMV并对胃机能进行调控呢?至今未见有文献报道。本研究通过向DMV微量注射AVP,观察对胃运动和胃酸分泌的影响来对这一问题进行探讨,并对其作用机制进行了初步研究。本文首先探讨了向DMV注射AVP对胃运动的影响,实验分两步: 第一步:观察大鼠右侧DMV微量注射AVP及AVP受体阻断剂对胃运动的影响。实验分四组:一组(对照组)右侧DMV注射生理盐水(0.2μL),二组右侧DMV注射0.18nmol AVP (0.2μL),三组右侧DMV注射0.018 nmol AVP(0.2μL),四组右侧DMV预先注射0.32 nmol AVP V1a受体阻断剂SR49059 (0.2μL),再向DMV注射0.018 nmol AVP(0.2μL)。用幽门部放置水囊的方法测定大鼠胃运动,观察注药前后的胃运动变化。统计指标包括注射前5min、注射后25min内胃的收缩幅度、时程以及胃运动指数,同时记录呼吸、血压、心电。结果:两种不同剂量的AVP被注射到右侧DMV后5min内,胃运动、呼吸、心率受到显著性抑制,平均血压无明显变化;随着时间的推移,AVP的抑制作用逐渐消失。但生理盐水被注射到右侧DMV后与注射前相比较,胃运动、呼吸、血压、心率均无明显改变。右侧DMV预先注射AVP V1a受体阻断剂SR49059,AVP对胃运动的抑制作用完全消除,这表明DMV中的AVP敏感神经元确实可抑制胃运动,且AVP的这种抑制作用是通过AVP V1a受体实现的。第二步是在第一步的基础上,通过预先股静脉注射植物性神经节胆碱能N1型受体阻断剂六烃季铵(8μmol,1mL),再向DMV注射AVP,用同样方法观察胃运动的变化,初步探讨了AVP在DMV内调控胃运动的神经元类型。结果:预先静脉注射六烃季铵后,胃运动几乎完全消失,平均动脉压显著降低,呼吸频率、心率无明显变化;待胃运动稍有恢复后,再向DMV内微量注射AVP,胃运动无明显变化。表明DMV内AVP敏感神经元对胃运动的调控是通过节前胆碱能神经元来实现的。本研究还探讨了AVP通过DMV对胃酸分泌的调控,实验分两组:一组(对照组)右侧DMV注射生理盐水(0.2μL),二组右侧DMV注射0.18 nmol AVP (0.2μL),通过食道插管灌流37℃生理盐水,幽门插管收集并用精密pH计测定灌流液,统计灌流液中的H+分泌量。结果:与注药前相比,注药后生理盐水组胃液H+分泌量无明显变化,AVP组胃液H+分泌量显著增加。这表明大鼠DMV微量注射AVP可促进胃液H+的分泌。结论:大鼠DMV内微量注射AVP可抑制胃运动,促进胃酸分泌。其调控机制可能为:AVP与DMV神经元胞体膜或树突膜上的AVP V1a型受体结合,通过节前胆碱能-节后NANC能抑制性迷走神经通路实现对胃运动的抑制性调控作用,通过节前胆碱能-节后胆碱能兴奋性神经通路实现对胃酸分泌的兴奋性调控作用。
[Abstract]:Rat rwis (restraint water-immersion, stress, RWIS) under the condition of gastric motility and gastric acid secretion dysfunction occurred. One of the more senior central in the regulation of gastrointestinal function in the anterior hypothalamus, supraoptic nucleus (SON), paraventricular nucleus (PVN) neurons in the most active, in the primary central medulla, dorsal nucleus of vagus nerve (DMV) neuronal activity is most intense, these results suggest that there may be SON to DMV and gastric nerve regulation loop exists. If there is, what is the neurotransmitter and its receptor, is still not clear. The known SON, PVN mainly by arginine vasopressin (AVP) and oxytocin (OT) can it has been reported that neurons, OT neurons have the nerve fiber ends at DMV to DMV; OT injection can inhibit gastric motility, stimulate gastric acid secretion, OT by DMV on the gastric function regulation, then, AVP neurons in the presence of DMV and the regulation of gastric function ? has not been reported in the literature. The research into DMV by microinjection of AVP, observe the effect on gastric motility and gastric acid secretion of this problem, and the mechanism was studied.
This paper first discusses the influence to the DMV injection of AVP on gastric motility, the experiment was divided into two steps:
The first step: To observe the rat right DMV microinjection of AVP and effect of AVP receptor antagonist on gastric motility. The experiment was divided into four groups: one group (control group) on the right side of the DMV injection of saline (0.2 L), the two group DMV injection of 0.18nmol AVP (0.2 L), the three group DMV injection of 0.018 nmol AVP (0.2 L), the four group DMV pre injection 0.32 nmol AVP V1a receptor antagonist SR49059 (0.2 L), and then to DMV injection of 0.018 nmol AVP (0.2 L). The gastric motility of rats determined by method of pylorus placed water sac, observe the changes of gastric motility before and after injecting the statistics. The index includes before injection of 5min, 25min in gastric contraction after the injection timing and the index of gastric motility, and record the breath, blood pressure, ECG. Results: two different doses of AVP were injected into the right DMV within 5min after gastric movement, breathing, heart rate was inhibited, the average blood pressure had no obvious change; with the passage of time, the inhibition of AVP Made gradually disappear. But the physiological saline was injected into the right after DMV compared with before injection, gastric motility, respiration, blood pressure, heart rate did not change significantly. Right DMV pre injection of AVP V1a receptor antagonist SR49059, inhibitory effect of AVP on gastric motility completely eliminated, suggesting that DMV in AVP sensitive neurons can inhibition of gastric motility, and the inhibitory effect of AVP was achieved by AVP V1a receptor.
The second step is on the basis of the first step in advance through femoral vein injection of autonomic ganglion cholinergic N1 receptor blocker hexamethonium six (8 mol, 1mL), and then to DMV injection of AVP, the changes of gastric motility were observed using the same method, discussed the types of neurons of AVP in regulation of DMV gastric motility. Results: pre intravenous injection of hexamethonium six, gastric motility is almost completely disappeared, the mean arterial pressure decreased, respiratory rate, heart rate had no significant change; to gastric motility recovered slightly after microinjection of DMV to AVP, gastric motility had no obvious change. That regulation of AVP sensitive neurons in DMV of stomach the movement is by preganglionic cholinergic neurons to achieve.
This study also investigated the AVP by DMV on the regulation of gastric acid secretion, were divided into two groups: one group (control group) on the right side of the DMV injection of saline (0.2 L), the two group DMV injection of 0.18 nmol AVP (0.2 L), through the esophageal intubation perfusion 37 C saline, collected and pyloric intubation meter perfusate with precision pH, statistics in the perfusate H+ secretion. Results: compared with before injection, injection of saline group after administration of H+ of gastric juice secretion had no obvious change, AVP group H+ of gastric juice secretion increased significantly. This indicated that DMV rats microinjection of AVP can promote the secretion of gastric juice H+.
Conclusion: rat DMV microinjection of AVP can inhibit gastric motility, and promote gastric acid secretion. The possible mechanism is: the combination of AVP and DMV neurons membrane or dendrites of AVP V1 type a receptor, cholinergic preganglionic postganglionic - by NANC can realize the inhibitory vagal pathway inhibitory effects on gastric motility. Through the pre - cholinergic postganglionic cholinergic excitatory neural pathway on excitability regulation of gastric acid secretion.

【学位授予单位】：山东师范大学
【学位级别】：硕士
【学位授予年份】：2011
【分类号】：R33

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