侧脑室注射TRH对大鼠胃内压的影响

大鼠侧脑室注射TRH10μg明显增加胃内压和引起较大幅度的胃的相位性收缩。延髓双侧迷走神经背核破坏后,TRH促进胃运动的效应减弱;双侧膈下迷走神经切断后,TRH的效应完全被阻断;外周注入阿托品也具有完全消除TRH效应的作用。本实验提示迷走神经背核是TRH中枢促进胃运动的一个重要神经结构,迷走神经是TRH效应的传出途径。     

微量注射6-OHDA损毁大鼠黑质对丘脑底核神经元电活动影响的研究

为了观察黑质内注射 6-OHDA损毁黑质多巴胺 (DA)能神经元后大鼠丘脑底核 (STN)神经元自发放电活动的变化 ,以探讨 STN神经元功能紊乱与帕金森病 (PD)运动障碍的关系 ,选择单侧黑质致密部 (SNC)微量注射 6-OHDA方法建立 PD大鼠模型 ,采用微电极细胞外记录神经元放电 ,观察对照组大鼠和 PD模型大鼠不同时期的 STN神经元放电频率及放电形式的变化。结果显示 ,对照组大鼠 STN神经元放电频率平均为 11.16± 1.5 2 Hz,其放电形式主要表现为规则型 (3 9/4 4) ,其次为混合型 (3 /4 4)和爆发型 (2 /4 4) ;而 PD模型大鼠 (SNC损毁 )不同时期的 STN神经元的放电形式发生明显变化 ,呈爆发型放电的神经元数较对照组大鼠明显增多 (P<0 .0 5和 P<0 .0 1) ;平均放电频率较对照组大鼠明显升高 (P<0 .0 5和 P<0 .0 1)。     

胃复春片对功能性消化不良大鼠胃肠功能的影响

目的 考察胃复春片对胃肠动力障碍的改善作用。方法 建立功能性消化不良（functional dyspepsia,FD）大鼠模型;以FD大鼠体质量、进食量、饮水量、胃平滑肌电活动情况、胃液分泌量、胃蛋白酶活性、肝脏与脾脏质量、胃病理情况等考察胃复春的药效。结果 模型组FD大鼠胃平滑肌电活动明显紊乱,体质量、进食量、饮水量明显减少、胃蛋白酶活性明显降低;经胃复春治疗后,上述现象明显缓解,大鼠体质量、进食量、饮水量明显增加,胃蛋白酶活性明显升高。结论 胃复春能改善FD大鼠的一般状况,对FD大鼠胃酸过多有抑制作用,能提高模型大鼠的胃蛋白酶活性。     

保留幽门和迷走神经的胃部分切除手术对早期胃癌的效果研究

目的 对应用保留幽门与迷走神经的胃部分切除术对患有早期胃癌的患者进行治疗的临床效果进行研究分析.方法 抽取72例患有早期胃癌的临床确诊患者病例,将其分为A、B两组,平均每组36例.分别采用常规胃部分切除手术和保留幽门与迷走神经的胃部分切除术进行治疗.结果 B组患者在围手术期内出现并发症的人数明显少于A组患者;该组患者的手术时间和住院治疗时间明显短于A组患者.结论 应用保留幽门与迷走神经的胃部分切除术对患有早期胃癌的患者进行治疗的临床效果非常突出.     

多柔比星诱导的心衰大鼠迷走神经的功能性改变

目的 探讨心衰大鼠迷走神经对心脏调节功能的变化以及电刺激迷走神经对心脏舒缩功能的影响。方法 将大鼠分为对照组、心衰模型组及迷走神经刺激组,对照组10只,每只给予生理盐水1 mL,心衰模型组及迷走神经刺激组共30只给予多柔比星腹腔注射2.5 mg·kg-1,每周1次,共6次。给药结束后行血流动力学检测、压力反射敏感性检测及迷走神经刺激(刺激频率:2.0 Hz,波宽:1.0 ms,刺激幅度:3 V,持续时间:240 min)。结果 与对照组相比,心衰组大鼠压力反射敏感性明显下降(n=10,3.29±0.47 vs 1.90±0.24,P＜0.05)。迷走神经刺激后,与心衰模型组大鼠比较,其左室舒张末压(LVEDP)明显降低(P＜0.01),而左室舒张期压力最大下降速率(-dP/dt_max)、左室等容收缩期压力最大上升速率(+dP/dt_max)、左室内压峰值(LVSP)均明显升高(均P＜0.01)。结论 多柔比星诱导的心衰大鼠迷走神经张力下降,电刺激迷走神经可明显改善心衰大鼠心脏的舒缩功能。迷走神经刺激有望成为治疗心力衰竭的有效方法之一。     

高选择性迷走神经切断术不附加引流治疗十二指肠溃疡病(文献综述)

一、历史简介:十二指肠溃疡患者多有迷走神经张力亢进和胃酸分泌过多的特点,1943年 Dvagstedt 首先应用迷走神经干切断术来治疗。由于全腹腔的迷走神经均被切断,术后常有顽固性腹泻、腹胀、倾倒综合症等副作用;又因胃窦失去迷走神经支配,蠕动减弱,幽门功能失常可致胃潴留。1945年 Dvagstedt 又提出应附加胃空肠吻合术,以解决胃排空机能障碍。1948年 Frankssom 报告了选择性迷走神经切断术,即保留迷     

门脉高压症贲门周围血管离断术不必附加幽门成形术

目的:探讨肝硬化门脉高压症病人行脾切除贲门周围血管离断术附加幽门成形术的必要性并观察保留迷走神经对胃排空功能恢复的影响。方法:观察肝硬化门脉高压症病人行脾切除贲门周围血管离断术双侧迷走神经主干切断组与保留迷走神经或附加幽门成形术组胃排空功能恢复情况。结果:双侧迷走神经主干切断组胃排空功能恢复平均时间5.2d,附加幽门成形术或保留迷走神经组分别为4.2d和4.1d。前者发生胃潴留2/36(6%)例,但均于短时间内恢复;后者未见胃潴留发生。结论:认为贲门周围血管离断术附加幽门成形术非为必需,术中保留迷走神经确属有益     

利用二氧化碳激光行大鼠的迷走神经切断的实验研究

高选择性迷走神经切断手术,较胃大部切除术简单、安全,是治疗十二指肠溃疡较理想的手术方法。但是,手术切断迷走神经,也还存在一些问题。由于解剖上的变异.导致神经切断不易完全,神经的荐生会造成一定的复发率,有时还会造成胃的缺血坏死。对此希望寻找一个既能切断迷走神经、又能克服上述手术的缺点、更简便有效的方法。我们利用二氧化碳激光照射鼠胃,控制一定的     

交感神经切除术在坐骨神经传入纤维中诱导新生的嘌呤能敏感性

目的:观察交感神经切除术是否可在大鼠坐骨神经传入纤维中诱导新生的嘌呤能敏感性.方法:应用单纤维记录技术在行交感神经切除术的大鼠坐骨神经上记录了32根A型传入纤维的自发放电活动;在正常鼠坐骨神经上记录了30根A类传入纤维的自发放电活动.通过颈静脉注射ATP(2 μmol).结果:行交感神经切除术的大鼠坐骨神经中28％自发放电纤维对ATP起反应,表现为放电频率增加或减少;而正常鼠坐骨神经中具有自发放电的纤维对ATP却均无反应.结论:交感神经切除术可在坐骨神经A类传入纤维中诱导新生的嘌呤能敏感性.     

实验性糖尿病大鼠心迷走神经及其心神经节结构变化的研究

目的对糖尿病心脏自主神经的病理生理变化进行深人研究,阐明糖尿病心脏自主神经病变的病理基础。方法采用神经示踪技术顺行标记实验性糖尿病大鼠模型的心迷走传出神经纤维及其支配的心脏神经节的神经纤维末端：同时采用荧光金染料标记心神经节神经元细胞,通过荧光显微镜和激光共聚焦显微镜观察其结构的改变。结果（1）糖尿病大鼠心脏神经元细胞胞体变小,细胞间隙模糊;（2）Dil标记的迷走神经传出纤维直径变细,伴局部肿胀：（3）被心脏迷走神经传出纤维所支配的心脏神经元细胞明显减少。结论糖尿病可导致心脏神经节细胞结构的改变,并减少迷走神经传卅纤维对神经节细胞的支配活动,这种改变可能与糖尿病患者心血管乐力反射敏感性的下降有关。     

The effect of clonidine on gastric acid secretion in rats and dogs

Summary The effect of clonidine on gastric acid secretion was investigated using rats and dogs. In the stomach lumen perfused rat basal gastric acid secretion was increased by clonidine in the anaesthetized rat but inhibited in the conscious animal. Clonidine also reduced the basal gastric acid secretion in rats with chronic gastric fistula, (ED₅₀ 12 g/kg p.o.). In addition, gastric secretion stimulated by insulin hypoglycaemia was inhibited by clonidine in anaesthetized stomach lumen perfused rats and in conscious dogs with gastric fistula. In the rat gastric secretion stimulated by electrical vagus stimulation was inhibited as well. However, clonidine had no effect on the gastric acid secretion stimulated by carbachol in stomach lumen perfused rats and in dogs with denervated fundic pouch.These results suggest that the inhibition of gastric acid secretion by clonidine probably is due to an inhibition of acetylcholine release at the vagus nerve endings. Additional central gastric antisecretory effects can, however, not be excluded by this study.     

Immunohistochemical and morphologic basis for glutamate signaling in the rat stomach

Physiologic studies conducted in rats have demonstrated that afferent fibers of the gastric branch of the vagus nerve increase their firing rate with the intragastric administration of the amino acid glutamate, and the increased firing rate is blocked by the depletion of serotonin (5-HT), administration of the blocker for the serotonin type-3 receptor (SR3), or nitric oxide synthase (NOS). To understand glutamate signaling in the gastric mucosa at the cellular level, we have been studying rats as an animal model using anatomic and immunohistochemical procedures. Our results have indicated that 5-HT-immunoreactive (ir) cells are present in the superficial part of the gastric mucosal epithelium and in the base of the fundic glands, whereas immunoreactivity for SR3 is localized in the neck and its vicinity of the fundic glands. Further, NOS1/neuronal NOS-ir cells with a bipolar shape are located in the lamina propria where a dense network of neuronal cells is present. These results suggest that complex cellular events take place during intragastric glutamate signaling.     

Substance P immunoreactivity in the rat mammary nipple and the effects of capsaicin treatment on lactation

Tissue concentrations of substance P immunoreactivity (SP-I) were measured in rat mammary nipples and were significantly greater than in ventral abdominal skin in nonpregnant and pregnant rats. In contrast, the concentration of nipple SP-I was lower than that of skin in twelve day lactating animals. The mean total SP-I content of the pooled twelve nipples from each rat was not significantly different in nonpregnant, pregnant or lactating rats. However, the mean weight of the pooled twelve nipples from each rat was significantly higher in the lactating rats than in pregnant rats. Immunohistochemistry revealed SP-I nerve trunks and single fibers throughout the nipples of lactating rats. Nerve fibers were observed among smooth muscle and along blood vessels throughout the dermis and in association with epidermal structures. Some SP-I fibers were also observed in association with the main lactiferous duct and mammary gland secretory parenchyma. Radioimmunoassay and immunohistochemistry of nipples from lactating rats treated with capsaicin as neonates revealed a marked depletion of SP-I. Rats treated with capsaicin as neonates had a normal gestation period and produced litters of normal size and birth weight. However, the litters of these lactating rats grew at a significantly slower rate than litters from controls. The quantity of milk obtained from capsaicin-treated lactating dams, following a one hour suckling period on the twelfth day of lactation, was significantly less than that obtained by litters of control dams. It is concluded that capsaicin-sensitive primary sensory nerves of the mammary nipple play a role in the afferent limb of the suckling reflex. One transmitter candidate for these nerves is substance P.     

Central site of inhibitory action of bombesin on gastric acid secretion in rats

Sites of inhibitory action of bombesin on gastric acid secretion were examined in rats anesthetized with urethane. Intracerebroventricular administration of bombesin (3-1000 pmole) dose-dependently inhibited the increase in gastric acid secretion induced by electrical stimulation of the vagus nerve (1 mA, 0.5 msec, 3 Hz). On the other hand, intrathecal (direct lumbar puncture) administration of bombesin, even in the large dose of 1 nmole, had no effect on the vagally stimulated gastric acid secretion. Three pmoles of bombesin microinjected into the preoptic area, the anterior hypothalamus and the paraventricular nucleus inhibited the vagus stimulated gastric acid secretion. Microinjection of this peptide into the ventromedial nucleus, the dorsomedial nucleus and the lateral hypothalamic area were without effect. A large electrolytic lesion of the anterior hypothalamus, including the preoptic-anterior hypothalamic area and the paraventricular nucleus, abolished the inhibitory effect of intracerebroventricularly applied bombesin, but a lesion restricted to the preoptic-anterior hypothalamus or the paraventricular nucleus was without effect. We propose that the preoptic area, the anterior hypothalamus and the paraventricular nucleus are all involved in the inhibitory effect of bombesin on gastric acid secretion.     

Stimulatory effect of centrally injected capsaicin, an agonist of vanilloid receptors, on gastric acid secretion in rats.

Capsaicin, the main pungent ingredient in chilli peppers, acts through specific vanilloid receptors on sensory neurons. The vanilloid receptors have been localized in the brain. We describe here a stimulatory effect of centrally injected capsaicin on gastric acid secretion in urethane-anesthetized rats. Injection of capsaicin (10-30 nmol per rat) into the lateral cerebroventricle markedly stimulated the secretion. Injection of capsazepine (30 nmol) or ruthenium red (30 nmol), antagonists for vanilloid receptors, into the lateral cerebroventricle inhibited the secretion induced by capsaicin, although these antagonists alone significantly stimulated the secretion. Injection of capsaicin into the fourth cerebroventricle also stimulated gastric acid secretion. The effects of centrally injected capsaicin into the lateral and fourth cerebroventricle were mediated via the vagus cholinergic nerve, because the effects were abolished by bilateral vagotomy at the cervical level. The present findings showed that central injection of capsaicin stimulated gastric acid secretion, via vanilloid receptors in the central nervous system (CNS), and through vagus nerve mechanisms in the perfused stomach of urethane-anesthetized rats.     

New therapeutic strategy for amino acid medicine: effects of dietary glutamate on gut and brain function

The gustatory and visceral stimulation from food regulates digestion and nutrient utilization, and free glutamate (Glu) release from food is responsible for the umami taste perception that increases food palatability. The results of recent studies reveal a variety of physiological roles for Glu. For example, luminal applications of Glu into the mouth, stomach, and intestine increase the afferent nerve activities of the glossopharyngeal nerve, the gastric branch of the vagus nerve, and the celiac branch of the vagus nerve, respectively. Additionally, luminal Glu evokes efferent nerve activation of each branch of the abdominal vagus nerve. The intragastric administration of Glu activates several brain areas (e.g., insular cortex, limbic system, and hypothalamus) and has been shown to induce flavor-preference learning in rats. Functional magnetic resonance imaging of rats has shown that the intragastric administration of Glu activates the nucleus tractus solitarius, amygdala, and lateral hypothalamus. In addition, Glu may increase flavor preference as a result of its postingestive effect. Considering these results, we propose that dietary Glu functions as a signal for the regulation of the gastrointestinal tract via the gut-brain axis and contributes to the maintenance of a healthy life.     

Chronic impairment of the vagus nerve function leads to inhibition of dopamine but not serotonin neurons in rat brain structures

BackgroundRecent clinical studies have shown that the dorsal motor nucleus of the vagus nerve is one of the brain areas that are the earliest affected by α-synuclein and Lewy body pathology in Parkinson's disease. This observation raises the question: how the vagus nerve dysfunction affects the dopamine system in the brain?MethodsThe rats underwent surgical implantation of the microchip (MC) in the abdominal region of the vagus. In this study, we examined the effect of chronic, unilateral electrical stimulation of the left nerve vagus, of two different types: low-frequency (MCL) and physiological stimulation (MCPh) on the dopamine and serotonin metabolism determined by high-pressure chromatography with electrochemical detection in rat brain structures.ResultsMCL electrical stimulation of the left nerve vagus in contrast to MCPh stimulation, produced a significant inhibition of dopamine system in rat brain structures. Ex vivo biochemical experiments clearly suggest that MCL opposite to MCPh impaired the function of dopamine system similarly to vagotomy.ConclusionWe suggest a close relationship between the peripheral vagus nerve impairment and the inhibition of dopamine system in the brain structures. This is the first report of such relationship which may suggest that mental changes (pro-depressive) could occur in the first stage of Parkinson's disease far ahead of motor impairment.     

l-alpha-Acetylmethadol administration to lactating rat dams. Effect on hepatic aniline hydroxylase and ethylmorphine N-demethylase activities in rat pups

l-alpha-Acetylmethadol (LAAM) was administered to lactating rat dams, and subsequent effects on hepatic drug-metabolizing enzymes of their offspring were assessed. Dams were given LAAM or a control solution in their drinking water following parturition and throughout lactation. Hepatic ethylmorphine-N-demethylase (EMDM) and aniline hydroxylase (AH) activities, as well as cytochrome P-450 content, were determined in the offspring at 21-23 days of age, or following sexual maturation (61-64 days). LAAM induced AH and EMDM activities, as well as cytochrome P-450 content in both male and female 21-23-day-old pups compared to controls; these differences were not observed at 61-64 days of age. In addition, normal sex-related differences in EMDM activity were apparent at 61-64 days of age. These results demonstrate the LAAM administration to lactating dams causes hepatic metabolic induction in the sexually immature rat, suggesting that LAAM and/or its metabolites passed to the pups via the milk. These changes, induced by LAAM administered via lactation, are reversible and do not interfere with the normal development of sex-dependent differences in hepatic EMDM activity observed in rats following sexual maturation.     

Effect of glycopyrronium bromide on basal, and histamine- or gastrin-induced gastric secretion

Acid secretory responses were obtained in rats given either intravenous histamine as dihydrochloride or gastrin subjected to partial purification. A continuous recording method for measuring gastric acid secretion was used. When the rat stomach was perfused with weak sodium hydroxide solution, glycopyrronium bromide (a powerful anticholinergic drug) blocked the acid gastric secretory effects of both histamine and gastrin. Glycopyrronium bromide in doses of 2 μg/100 g body weight of rat is well tolerated. Doses higher than 2 mg/100 g caused respiratory disturbances. The action of glycopyrronium bromide in blocking the gastric secretory effects of gastrin supports the hypothesis that gastrin acts partly by stimulating the vagus nerve.     

Factors related to increased susceptibility to intestinal lesions with nonsteroidal anti-inflammatory agents in the lactating rat

The toxic response to carprofen, a nonsteroidal anti-inflammatory agent, was found to be 1.7 times greater in lactating rats as compared to control nulliparous female rats. A study of enterohepatic function and the biliary excretion of carprofen during lactation showed large physiological differences between lactating and control female rats. Marked increases in food consumption (three- to fourfold), bile flow (twofold), liver weights (twofold), small intestine weights (twofold), and small intestinal β-glucuronidase activity (fourfold) were observed. A study of biliary excretion of [¹⁴C]carprofen showed that unchanged carprofen and its major metabolites (phenolic derivatives) are excreted almost entirely as conjugates. The biliary excretion tended to be higher in the lactating rat in which 46.7% of a 5 mg/kg iv dose was excreted in 4 hr as compared to 38.6% in controls. In terms of absolute amounts of unchanged carprofen excreted into the intestine the lactating rat excreted approximately 1.5 times more. The metabolite patterns were not substantially different in the lactating rat. Some of these factors including increased food residue in the intestine, increased excretion of intact drug and increased β-glucuronidase activity, would be expected to at least contribute to, if they are not responsible for, the increased susceptibility to the toxicity of nonsteroidal anti-inflammatory agents during lactation.