Relaxation Of Proximal Stomach Research Articles

Effect of antidepressant treatment on water load test and cortisol changes in patients with functional dyspepsia

Background It has been demonstrated that patients with functional dyspepsia have experiences social life stress events, and accompanied by psychological disorders, mainly manifested as depression and anxiety. Mental factors can lead to excessive gastrointestinal consensual reaction, and result in different brain-gut axis disturbance, and then cause the gastrointestinal sensorimotor abnormality and endocrine changes. Objective To observe the effect of antidepressant treatment on the changes of water load and serum cortisol in patients with functional dyspepsia, and analyze the therapeutic mechanism. Design A comparative observation. Setting The First Affiliated Hospital o Zhengzhou University. Participants Forty-five patients with functional dyspepsia accompanied by depression were selected from the Department of Gastroenterology, the First Affiliated Hospital of Zhengzhou University from July 2004 to July 2006, and they were 25–65 years of age, and their disease courses ranged 1–10 years. They were all accorded with the diagnostic standards for Rome II functional dyspepsia functional dyspepsia. As the patients' will, they were divided into treatment group ( n =30, 12 males and 18 females) and control group ( n =15, 6 males and 9 females), and there were no significant differences in the data between the two groups ( P > 0.05). The programs were discussed and agreed by the committee of medical ethics of the First Affiliated Hospital of Zhengzhou University. Informed contents were obtained from all the patients. Methods In the treatment group, the patients were treated with venlafaxine sustained release capsule (75 mg per day), and those with sleep disorder were added by benzodiazepines (alprazolam). In the control group, the patients were given routine treatments of antacid, prokinetics, etc. Before and after 8-week treatment, the following examinations were performed: ▪ The gastrointestinal symptoms were assessed according to the symptoms; ▪ The severity of depression was evaluated with Hamilton depression scale (HAMD); ▪ The relaxation of proximal stomach was observed using water load test; ▪ The serum level of cortisol was detected. Main outcome measures ▪ Symptom score; ▪ HAMD score; ▪ Water load amount; ▪ Serum level of cortisol. Results All the 45 patients were involved in the analysis of results. ▪ Symptom score: The scores of gastrointestinal symptoms were decreased as compared with those before treatment in both the treatment group and control group ( P < 0.05). ▪ HAMD scores: The scores of HAMD were decreased as compared with those before treatment in both the treatment group and control group ( P < 0.05). ▪ Water load amount: The total effective rate was significantly higher in the treatment group than the control group ( P < 0.05). ▪ The serum levels of cortisol after treatment were significantly lower than those before treatment in the patients with severe gastrointestinal symptoms in the treatment group and control group ( P < 0.05). Conclusion Antidepressants can normalize the cortisol level of patients with functional dyspepsia, and then decrease gastric sensitivity and ameliorates the receptive relaxation of proximal stomach, also increase the water load amount correspondingly, and finally control the gastrointestinal symptoms of functional dyspepsia.

Effects of Ondansetron on Gastric Tone and Motility Changes Induced by a Prolonged Intraduodenal Infusion of Nutrients. Results of a Placebo-Controlled Study

Our aim was to study the 5-HT3 antagonist, ondansetron, on gastric motility changes induced by duodenal infusion of nutrients. First, the effects of a 2-hr intraduodenal infusion (IDI) of a caloric diet on antral motility were assessed. Second, a crossed-over placebo-controlled study assessed 3-day oral intake of ondansetron (8 mg bid) on gastric motility changes induced by the IDI. During the IDI, antral numbers of waves (NW) as area under curve (AUC) were lower than fasting values. After infusion, antral NW and AUC increased to return to basal values. The antral area increased slightly shortly after the start of the IDI, then remained stable. When subjects received ondansetron, the only significant motor effect was a higher antral NW and AUC during the first 30 min of the IDI (P < 0.05). After the end of the IDI, the AUC and NW increased in both the distal and the proximal antrum. The increase was lower by ondansetron in the proximal antrum. Proximal stomach relaxation induced was not influenced by ondansetron. In conclusion, an IDI of nutrients decreased antral motility, increased the antral area, and promoted fundic relaxation. This inhibitory effect was rapidly reversible. Ondansetron induced only minor motility changes in the antrum and had no effect on fundic relaxation promoted by IDI.

Effects of Intragastric L-Arginine Administration on Proximal Stomach Tone Under Basal Conditions and After an Intragastric Diet

Nitric oxide (NO) plays an important role as a nonadrenergic, noncholinergic inhibitory neurotransmitter in the GI tract. Our study aims were to investigate the effect of a single intragastric L-arginine (L-Arg) administration, as a source of NO, on proximal stomach tone in basal and postintragastric administration of a polymeric diet in humans and to evaluate concomitantly the effect on antral area as an indirect assessment of gastric emptying. Eight healthy volunteers were studied in a randomized double-blind crossover study after, respectively, 15 g L-Arg, 30 g L-Arg, or placebo administered in the stomach through a gastric tube. The drug administration was followed by a polymeric diet infusion (500 ml/500 kcal) at a rate of 250 ml/hr. Gastric tone variations were recorded with an electronic barostat, gastric emptying was concomitantly estimated by repeated ultrasound measurements of antral area, and symptoms were recorded throughout the experiment.L-Arg administration was associated with significantly higher increases in barostat bag volumes at both dosages, 30 g (117+/-16 ml) and 15 g (67+/-15 ml), compared to placebo (46+/-11 ml; P < 0.05). In response to the polymeric diet the 30-g L-Arg challenge was associated with a smaller increase in intrabag volume, whereas postinfusion final volumes did not differ in the three treatment conditions. Antral areas were not different at any time of measurement among the three challenges. Bloating and diarrhea were observed after 30-g L-Arg administration in five subjects of eight. Short-term L-Arg administration was able to induce proximal stomach relaxation that allowed a secondary response to enteral feeding only at the 15-g dosage. This 15-g dosage was as well tolerated as the placebo and was associated with no significant changes in gastric emptying patterns.

Central neuropeptide Y induces proximal stomach relaxation via Y1 receptors in the dorsal vagal complex of the rat

Effects of neuropeptide Y (NPY) on motility of the proximal stomach was examined in anesthetized rats. Intragastric pressure was measured using a balloon situated in the proximal part of the stomach. Administration of NPY into the fourth ventricle induced relaxation of the proximal stomach in a dose-dependent manner. Administration of an Y1 receptor (Y1R) agonist [Leu31, Pro34]NPY induced a larger relaxation than NPY. The administration of an Y2 receptor agonist (NPY 13-36) did not induce significant changes in motility. Microinjections of [Leu31, Pro34]NPY into the caudal part of the dorsal vagal complex (DVC) induced relaxation of the proximal stomach. In contrast, similar injections into the intermediate part of the DVC increased IGP of the proximal stomach. Administration of NPY into the fourth ventricle did not induce relaxation after bilateral injections of the Y1R antagonist (1229U91) into the caudal DVC. These results indicate that NPY induces relaxation in the proximal stomach via Y1Rs situated in the DVC. Because bilateral vagotomy below the diaphragm abolished the relaxation induced by the administration of NPY into the fourth ventricle, relaxation induced by NPY is probably mediated by vagal preganglionic neurons. Intravenous injection of atropine methyl nitrate reduced relaxation induced by administration of NPY. Therefore, relaxation induced by NPY is likely mediated by peripheral cholinergic neurons.

Characterization of 5-HT7-receptor-mediated gastric relaxation in conscious dogs

We aimed to evaluate the gastric relaxant capacity of the 5-HT(1/7)-receptor agonist 5-carboxamidotryptamine (5-CT) in conscious dogs and to clarify the mechanism of action by use of selective antagonists, vagotomy, and in vitro experiments. A barostat enabled us to monitor the intragastric volume in response to different treatments (intravenously administered) before and after supradiaphragmatic vagotomy [results presented as the maximum volume change after treatment (mean; n = 5-11)]. In vitro experiments were performed with isolated muscle strips cut from four different stomach regions of the vagotomized dogs [results were fitted to the operational model of agonism to determine the efficacy parameter tau (n = 5)]. 5-CT (0.5-10 microg/kg) caused a dose-dependent gastric relaxation (29-267 ml) that was completely blocked by the selective 5-HT(7)-receptor antagonist SB-269970 (50 microg/kg). After vagotomy, the relaxation to 10 microg/kg 5-CT was significantly less pronounced (73 vs. 267 ml; P < 0.05) but still blocked by SB-269970, whereas the response to the nitric oxide donor nitroprusside was similar to that before vagotomy (178 vs. 218 ml). In vitro, 5-CT concentration dependently inhibited the PGF(2alpha)-contracted muscle strips before and after vagotomy. Although before and after vagotomy the response in every region was mediated by 5-HT(7) receptors (apparent affinity dissociation constant: SB-269970, 8.2-8.6 vs. 8.3-8.6, respectively), the response after vagotomy was less efficacious (log tau: 1.9 to 0.5 vs. 1.4 to -0.1). The results indicate that the 5-CT-induced proximal stomach relaxation in conscious dogs before and after vagotomy is mediated via 5-HT(7) receptors. The decreased efficacy of 5-CT in vitro after vagotomy is probably related to vagotomy-induced changes in receptor density or coupling efficiency and provides a possible explanation for the decreased in vivo response to 5-CT after vagotomy.

Mechanisms of insulin-induced relaxation of the canine proximal stomach after proximal gastric vagotomy

The aim of this study was to determine whether insulin-induced relaxation of the proximal stomach after proximal gastric vagotomy is mediated by vagal release of antral gastrin. In six conscious, fasted dogs following proximal gastric vagotomy, the effects of intravenous insulin (1 U/kg) and intravenous gastrin (1 μg/kg) on proximal gastric motility, as measured by a gastric barostat, on plasma glucose, and on plasma gastrin, as measured by radioimmunoassay, were assessed 1 hour before and for 2 hours after injection. The effects of a cholecystokinin (CCK)-A receptor antagonist and a CCK-B receptor antagonist on insulin-induced or gastrin-induced relaxation of the proximal stomach and on plasma glucose and gastrin were also determined. Intravenous insulin decreased plasma glucose (before [mean ± SD], 97 ± 5 mg/dl vs. after, 45 ± 3 mg/dl; P <0.05), increased plasma gastrin (before, 240 ± 59 pg/ml vs. peak after, 387 ± 85 pg/ml; P <0.05), and relaxed the proximal stomach (100% ± 0% barostat volume vs. 202% ± 15% volume; P <0.05). Exogenously administered gastrin also relaxed the proximal stomach without decreasing plasma glucose. CCK-B blockade diminished, but did not abolish, the gastric relaxation caused by insulin or gastrin, whereas CCK-A blockade had little effect. It was concluded that insulin-induced relaxation of the proximal stomach after proximal gastric vagotomy is mediated, in part, by vagal release of antral gastrin.