gastrins and Jejunal-Diseases

Exogenous infusion of acid into the canine duodenum inhibits acid secretion stimulated by endogenously released and exogenously administered gastrin. The importance of this mechanism in normal acid homeostasis and in the inhibition of chronic endogenous acid hypersecretion is not established. In this study the classic Dragstedt model antral colonic transplant (ACT) was used to produce endogenous hypergastrinemia and acid hypersecretion. The effects of the ACT when the duodenum was retained in continuity with the stomach (gastroduodenostomy) were compared with those obtained when the duodenum was no longer in continuity with the stomach (gastrojejunostomy). The duodenum markedly suppressed gastrin release (p = 0.003) and gastric acid secretion (p = 0.005) in each of the four dogs. The dogs remained free of ulcers for 8 months after gastroduodenostomy and ACT. However, after conversion to gastrojejunostomy, large, chronic peptic ulcers developed after a mean of 3.5 months. The inhibitory effect of the duodenum on gastric release and gastric acid secretion protected the dog against ulceration for an extended period. The duodenum may be the major site of inhibitory control of acid secretion and endogenous gastrin release in dogs.

Topics: Anastomosis, Surgical; Animals; Colon; Dogs; Duodenum; Gastric Acid; Gastric Acidity Determination; Gastrins; Jejunal Diseases; Jejunum; Models, Biological; Pentagastrin; Postoperative Complications; Pyloric Antrum; Stomach

Topics: Calcium; Diagnosis, Differential; Duodenal Ulcer; False Negative Reactions; False Positive Reactions; Gastrectomy; Gastrins; Humans; Infusions, Parenteral; Injections, Intravenous; Jejunal Diseases; Peptic Ulcer; Secretin; Stomach Ulcer; Time Factors; Zollinger-Ellison Syndrome

The effectiveness of cimetidine or antacid in healing recurrent jejunal peptic ulcers after Billroth II gastric resection without vagotomy was tested in a randomized study of 18 in-patients. Mean stimulated acid secretion of the cimetidine group was 11.2 +/- 4.3 mmol/h, in the antacid group 12.6 +/- 5.6 mmol/h. Serum gastrin levels were within the normal range in all patients. Within four weeks the ulcers had healed completely in eight of the nine patients on cimetidine (1,000 mg/d), but in only three of the nine patients on antacids (magnesium-aluminiumhydroxide, neutralization capacity 564 mmol/d). The difference is statistically significant (P less than 0.025). All 11 patients with healed ulcers were given prophylactically either 800 mg cimetidine daily or magnesium-aluminiumhydroxide (neutralization capacity 564 mmol/d). During a follow-up period of one year recurrences occurred in two of the five patients on antacids, but in none of the six treated with cimetidine. The results indicate that cimetidine also accelerates the healing of recurrent jejunal peptic ulcers. But further studies are required to elucidate whether long-term treatment with histamine-H2-receptor antagonists is as good as surgery in the long-term prevention of ulcer recurrences.

Topics: Adult; Antacids; Cimetidine; Female; Gastrectomy; Gastrins; Guanidines; Humans; Jejunal Diseases; Male; Middle Aged; Peptic Ulcer; Postoperative Complications; Recurrence

Topics: Adult; Gastric Juice; Gastrins; Humans; Intestinal Fistula; Jejunal Diseases; Male; Recurrence; Ulcer

The aim of this study was to determine whether mucosal antrectomy, which preserves antropyloric motility, would enhance the antiulcer properties of proximal gastric vagotomy (PGV). Hydrochloric acid and gastrin secretion were studied in five dogs before and after PGV and mucosal antrectomy, while the response to the Mann-Williamson operation (an ulcer-producing operation) was evaluated in four control dogs with intact stomachs, five dogs with PGV alone, and six dogs with PGV plus mucosal antrectomy. Proximal gastric vagotomy and mucosal antrectomy decreased mean +/- SEM basal and pentagastrin-stimulated acid secretion from 4.3 +/- 1.3 to 0.4 +/- 0.3 mEq/hr and from 21 +/- 0.7 to 7.4 +/- 1.8 mEq/hr, respectively (p less than 0.05). Basal plasma gastrin was altered little by the operation (68 +/- 9.7 pg/ml before, 58 +/- 11 pg/ml after; p greater than 0.05) but the 4-hour integrated plasma gastrin response to a 200 gm meat meal decreased from 13 +/- 1.8 to 3.3 +/- 0.7 ng X min/ml (p less than 0.05). Only one of six dogs with mucosal antrectomy and PGV developed peptic ulcer after the Mann-Williamson operation, whereas four of five with PGV alone and three of four controls developed ulcers (p less than 0.05, PGV alone versus PGV and mucosal antrectomy). In conclusion, PGV and mucosal antrectomy decreased acid secretion and postcibal gastrin response and provided greater protection against peptic ulcer than PGV alone.

Topics: Animals; Dogs; Evaluation Studies as Topic; Female; Gastric Acid; Gastric Mucosa; Gastrins; Jejunal Diseases; Male; Peptic Ulcer; Postoperative Complications; Pyloric Antrum; Vagotomy, Proximal Gastric

The mucosal concentrations of seven regulatory peptides and the density properties and integrity of their storage granules have been studied in mucosal biopsies from the human jejunum in eight gastrointestinal disease states and compared with normal controls. In diseases with associated mucosal inflammation (coeliac disease, Crohn's disease with jejunal involvement, postinfective tropical malabsorption, and common variable immunodeficiency) there was a selective increase in fragility of the gastric inhibitory polypeptide (GIP) and somatostatin storage granules. The gastrin, motilin, enteroglucagon, secretin, and vasoactive intestinal polypeptide granules had normal properties in these conditions. In diseases in which diarrhoea occurred in the absence of changes in jejunal mucosal histology (irritable bowel syndrome, pancreatic insufficiency, jejuno-ileal bypass for morbid obesity, and purgative abuse) there were no abnormalities of the storage granules. Increased mucosal concentrations of all peptides except vasoactive intestinal polypeptide (VIP) were found in coeliac disease and selective increases of VIP found in Crohn's disease, motilin in the irritable bowel syndrome and gastrin and GIP in pancreatic insufficiency. It is suggested that the storage granule abnormalities in the diseases with abnormal mucosal histology are secondary to the inflammatory changes.

Topics: Gastric Inhibitory Polypeptide; Gastrins; Gastrointestinal Hormones; Glucagon-Like Peptides; Humans; Intestinal Mucosa; Jejunal Diseases; Motilin; Secretin; Somatostatin; Vasoactive Intestinal Peptide

The effects of jejunal ulcer and chronic endogenous hypergastrinemia on canine gastrointestinal myoelectric activity were investigated in three groups of dogs. All dogs were chronically implanted with electrodes on the stomach and either the duodenum or jejunum. Fasted-state myoelectric activity was monitored before and after gastroenterostomy. Two groups of dogs underwent autotransplantation of the gastric antrum to the midcolon with either gastroduodenostomy or gastrojejunostomy. The third group of dogs underwent diversion of the antroduodenum with gastrojejunostomy. Chronic hypergastrinemia was observed postoperatively in the dogs of each of the three models. Only dogs with gastrojejunostomy and antrocolic transplant developed intestinal ulcers. None of the dogs, despite the presence of ulcers in one group, demonstrated significant changes in myoelectric activity. In both gastrojejunostomy models, a trend toward lengthened interdigesive phase 2 at the expense of phase 1 was seen. No other myoelectric changes were observed and chronic hypergastrinemia had no effect on myoelectric activity in these models. We conclude; (a) experimental jejunal peptic ulcer is not marked by significant changes in interdigestive myoelectric activity and (b) chronic hypergastrinemia is not accompanied by the gastrointestinal muscle, effects reported after acute treatment with gastrin, suggesting a tolerance.

Topics: Animals; Dogs; Electrophysiology; Female; Gastrins; Gastrointestinal Motility; Jejunal Diseases; Male; Muscle Contraction; Muscle, Smooth; Peptic Ulcer

In a pancreatic adenoma approximately 78.7% of the endocrine cells reacted specifically with antisera to neurotensin, 17.5% to gastrin, 2.8% to pancreatic polypeptide, and 1% to glucagon. The electron microscope revealed that the majority of the endocrine cells were N-cells--morphologically similar to the ileal N-cells which are known to represent the neurotensin-producing cells. Neurotensin was extracted from the tumor and identified by Sephadex, ion-exchange, and high-pressure liquid chromatography. Gastrin, pancreatic polypeptide, and glucagon cells were also identified by the electron microscope; the peptides were extracted and demonstrated by chromatography. The serum concentrations of these hormones were elevated. After total gastrectomy which was necessary because of Zollinger-Ellison syndrome, a jejunoesophageal alkaline reflux, reaching the upper esophagus appeared. As intravenous infusion of synthetic neurotensin in rats caused an increase of luminal enteric pressure, it is suggested that severe jejunoesophageal reflux after gastrectomy may be a clinical feature of a neurotensinoma.

Topics: Adenoma; Adult; Esophagitis, Peptic; Gastrins; Glucagon; Histocytochemistry; Humans; Jejunal Diseases; Male; Neurotensin; Pancreatic Neoplasms; Pancreatic Polypeptide

A review of 42 patients with gastrinoma, who either survived five years or longer or who died during this period of evaluation, was carried out to define the surgical principles which might be combined with the recent trend toward cimetidine therapy. Thirty-four (80%) of the patients had total gastrectomy with an operative mortality rate of 2.3%, and eight patients (20%) had less than total gastrectomy. No tumor was found in six patients with hypergastrinemia and an abnormal secretin bolus whose five-year survival rate was 100%. Of the thirty-six patients having tissue proof of gastrinoma, twenty-two (61%) had complete resection of all gross tumor resulting in a 76% five-year survival rate. Fourteen patients had unresectable tumor or partial resection with a five-year survival rate of 21%. Complete gross tumor resection increased mean survival by six years (p < 0.01), but resulted in persistent eugastrinemia in only two patients. Long-term survival was possible with a combination of vagotomy, lesser gastric procedures, tumor resection, and cimetidine, seven of eight patients living more than five years. Surgical management of gastrinoma should be directed toward aggressive tumor resection and vagotomy, with reliance on cimetidine therapy postoperatively to control the gastric hypersecretion. Total gastrectomy should be reserved for cimetidine failures and those who do not wish to take cimetidine for the rest of their lives.

Topics: Adenoma, Islet Cell; Cimetidine; Follow-Up Studies; Gastrectomy; Gastrins; Humans; Jejunal Diseases; Pancreatectomy; Pancreatic Neoplasms; Peptic Ulcer; Vagotomy