Cholinergic regulation of human proximal duodenal mucosal bicarbonate secretion

1991 ◽  
Vol 261 (2) ◽  
pp. G327-G331 ◽  
Author(s):  
M. A. Ballesteros ◽  
J. D. Wolosin ◽  
D. L. Hogan ◽  
M. A. Koss ◽  
J. I. Isenberg

Cephalic-vagal stimulation affects a number of upper gastrointestinal secretory and motility events. The purpose of this study was to examine the role of vagal-cholinergic regulation on human proximal duodenal mucosal HCO-3 secretion. The duodenal bulb was isolated between balloons and perfused with 154 mM NaCl, and HCO-3 secretion was measured. Although cholinergic stimulation with bethanechol (50 micrograms.kg-1.h-1 iv) produced systemic effects, resting HCO-3 secretion was unchanged. Cephalic-vagal stimulation, induced by sham feeding, significantly increased duodenal HCO-3 secretion from a basal of 177 +/- 17 to 240 +/- 19 mumols.cm-1.h-1 (P less than 0.02). The response to sham feeding was approximately 50% of the peak response to acid-stimulated HCO-3 output. Atropine (22 micrograms/kg iv) inhibited basal HCO-3 secretion significantly (79 +/- 5%). However, the net incremental increases in duodenal mucosal HCO-3 secretion in response to luminal acidification and vagal stimulation were unaltered by atropine pretreatment. Additionally, indomethacin (100 mg po) failed to modify the response to vagal-stimulated HCO-3 secretion. These findings indicate that basal human proximal duodenal mucosal HCO-3 secretion is maintained largely by resting cholinergic innervation and is stimulated by cephalic-vagal stimulation. Furthermore, since the incremental HCO-3 responses to cephalic-vagal stimulation and luminal acidification were unaltered by atropine pretreatment, each is likely mediated by noncholinergic mechanisms.

1993 ◽  
Vol 265 (2) ◽  
pp. G270-G276 ◽  
Author(s):  
H. S. Odes ◽  
R. Muallem ◽  
R. Reimer ◽  
W. Beil ◽  
M. Schwenk ◽  
...  

Although it is well known that vagal stimulation induces duodenal HCO3- secretion, there is presently no information about the nature of the cholinoceptor and the intracellular signals involved. In a series of experiments performed in a guinea pig duodenal loop model in situ, intravenous carbachol, atropine, pirenzepine, and hexamethonium were used to determine the extent of cholinergic stimulation and the types of cholinoceptors. Carbachol (2 micrograms.kg-1.5 min-1) stimulated HCO3- secretion threefold, and atropine (0.1 mg.kg-1.5 min-1) and pirenzepine (1 mg.kg-1.5 min-1) both abolished this effect. In addition, hexamethonium (0.3 mg.kg-1.5 min-1) inhibited carbachol-stimulated duodenal HCO3- secretion. Vasoactive intestinal peptide (VIP, 5 micrograms.kg-1.5 min-1) stimulated duodenal HCO3- secretion, and this action was partly inhibited by atropine (0.1 mg.kg-1.5 min-1) but not by pirenzepine (1 mg.kg-1.5 min-1). [4Cl-D-Phe6,Leu17]VIP (3.3 mg/kg), an antagonist to VIP, reduced basal, VIP-stimulated, and carbachol-stimulated HCO3- secretion. To examine the role of Ca2+ in this process, Ca2+ ionophore A23187, verapamil, and nifedipine were employed. A23187 (5, 50, 500 micrograms.kg-1.5 min-1) stimulated duodenal HCO3- secretion, an effect blocked by the VIP antagonist, and modestly augmented the effect of carbachol. Verapamil (0.2 mg.kg-1.5 min-1) and nifedipine (1.7 mg.kg-1.5 min-1) stopped the effect of carbachol on duodenal HCO3- secretion. These results suggest, that in cholinergic regulation of duodenal HCO3- secretion, the M-cholinoceptor pathway, Ca2+, and VIP are involved.


1990 ◽  
Vol 258 (6) ◽  
pp. G919-G925 ◽  
Author(s):  
B. I. Hirschowitz ◽  
J. Fong

In four gastric-fistula dogs, selective antral vagotomy markedly reduced the vagal stimulation of gastrin release, thereby defining both the vagal pathway for stimulation of gastrin and the anatomic source of such gastrin release. Despite loss of gastrin response, vagal excitation by 100 mg/kg 2-deoxy-D-glucose (2-DG) produced the same acid and pepsin responses after antral vagotomy as before, but there was an approximately 40% diminished fundic response to pentagastrin, histamine, and synthetic human gastrin, as well as to endogenous gastrin released by graded doses of bombesin. Bethanechol did not reverse the defect, ruling out inadvertent fundic vagal denervation, nor did raising serum gastrin by bombesin alter the response to vagal stimulation by 2-DG. Fundic response to bethanechol was increased by approximately 60%, and the output of gastrin increased at least fivefold after antral vagotomy. Gastrin responses to food were diminished and those to sham feeding were eliminated. Separation of the denervated antral pouch had no additional effect on acid secretion. Vagal stimulation of gastric secretion thus occurs almost exclusively through direct cholinergic effects on the fundus with little or no contribution from antral gastrin. Vagal denervation sensitizes the antrum to cholinergic stimulation.


2021 ◽  
pp. 332-337
Author(s):  
Heasty Oktaricha ◽  
Muhammad Miftahussurur

Double pylorus, also known as acquired double pylorus, is a rare condition defined as a gastrointestinal fistula connecting stomach antrum and duodenal bulb. The prevalence of double pylorus ranges from 0.001 to 0.4% by esophagogastroduodenoscopy (EGD). Although the etiology is unknown, the formation of double pylorus is related to Helicobacter pylori infection and the use of non-steroidal anti-inflammatory drugs (NSAID). The development of the occurrence of double pylorus is still unknown, but many systemic diseases play a role. We present the case of a 59-year-old man who was admitted to Dr. Soetomo General Hospital with hematemesis and melena. The patient had a history of diabetes mellitus since 3 years and consumption of medicinal herbs for myalgia, which was suspected of NSAIDs for the past 5 months. The patient had anemia with hemoglobin at 8.3 g/dL, enterogenous azotemia with blood urea nitrogen 28 mg/dL and serum creatinine 1.14 mg/dL. At EGD, double pylorus was found and accompanied by gastric ulcer, a giant white base ulcer, part of it covered by clotting without any sign of active bleeding. Biopsy revealed chronic inactive gastritis, and no H. pylori was found. Treatment mainly depends on gastrointestinal acid suppression through a proton pump inhibitor (PPI). The patient was given a high-dose PPI and a mucosal protective agent. He was treated for 1 week and had improved complaints.


2002 ◽  
Vol 14 (4) ◽  
pp. 152-155 ◽  
Author(s):  
Carlos A. Cappellanes ◽  
Kiyoshi Hashiba ◽  
Horus A. Brasil ◽  
Marco A. D’Assunção ◽  
Daniel Moribe ◽  
...  

Chemotherapy ◽  
2017 ◽  
Vol 62 (5) ◽  
pp. 290-294 ◽  
Author(s):  
Geng-Yuan Zhang ◽  
Jie Mao ◽  
Bin Zhao ◽  
Bo Long ◽  
Hao Zhan ◽  
...  

Duodenal bulb adenocarcinoma is an extremely rare malignancy in the alimentary tract which has a low incidence rate and nonspecific symptoms. It is difficult to diagnose early, and the misdiagnosis rate is high. CT, MRI, upper gastrointestinal endoscopy, and other advanced imaging modalities should be combined to make a comprehensive evaluation. The diagnostic confirmation of this tumor type mainly depends on the pathological examination. The combination of surgery with other treatment modalities is effective. A review of reports on duodenal bulb adenocarcinoma with chemotherapy revealed 6 cases since 1990. However, there are few reports on neoadjuvant chemotherapy for the disease. In this report, preoperative S-1 in combination with oxaliplatin neoadjuvant chemotherapy achieved a complete pathological response in the treatment of duodenal bulb adenocarcinoma. Neoadjuvant chemotherapy shows a better clinical efficacy in the treatment of duodenal bulb adenocarcinoma, but its value needs to be further verified.


2006 ◽  
Vol 290 (1) ◽  
pp. G23-G29 ◽  
Author(s):  
Marie-Claude L'Heureux ◽  
Ahmad Muinuddin ◽  
Herbert Y. Gaisano ◽  
Nicholas E. Diamant

The lower esophageal sphincter (LES) has a circular muscle component exhibiting spontaneous tone that is relaxed by nitric oxide (NO) and a low-tone sling muscle that contracts vigorously to cholinergic stimulation but with little or no evidence of NO responsiveness. This study dissected the responses of the sling muscle to nitrergic innervation in relationship to its cholinergic innervation and circular muscle responses. Motor responses were induced by electrical field stimulation (EFS; 1–30 Hz) of muscle strips from sling and circular regions of the feline LES in the presence of cholinergic receptor inhibition (atropine) or NO synthase inhibition [ NG-nitro-l-arginine (l-NNA) ± atropine]. This study showed the following. First, sling muscle developed less intrinsic resting tone compared with circular muscle. Second, with EFS, sling muscle contracted (most at ≤10 Hz), whereas circular muscle relaxed >50% by 5 Hz. Third, on neural blockade with atropine or l-NNA ± atropine, 1) sling muscle, although predominantly influenced by excitatory cholinergic stimulation, had a small neural NO-mediated inhibition, with no significant non-NO-mediated inhibition and 2) circular muscle, although little affected by cholinergic influence, underwent relaxation predominantly by neural release of NO and some non-NO inhibitory influence (at higher EFS frequency). Fourth, the sling, precontracted with bethanecol, could relax with NO and some non-NO inhibition. Finally, the tension range of both muscles is similar. In conclusion, sling muscle has limited NO-mediated inhibition to potentially augment or replace sling relaxation effected by switching off its cholinergic excitation. Differences within the LES sling and circular muscles could provide new directions for therapy of LES disorders.


2016 ◽  
Vol 31 (3) ◽  
pp. 470-478 ◽  
Author(s):  
Dong-Won Ahn ◽  
Young Soo Park ◽  
Sang Hyub Lee ◽  
Cheol Min Shin ◽  
Jin-Hyeok Hwang ◽  
...  

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