Gastric acid secretory differences in patients with Heineke-Mikulicz and Finney pyloroplasties

To study gastric emptying and secretion, liquid meals of 10% glucose lasting 15 and 30 min, and physiological saline meals lasting 30 min, all containing phenol red as a gastric nonabsorbable marker, were given to postvagotomy patients with Finney or Heineke-Mikulicz pyloroplasties. No differences in emptying were found. A small but statistically greater amount of acid was found in the stomach with the 15-min glucose meal after Heineke-Mikulicz pyloroplasty. This represented greater acid secretion into glucose meals generally after Heineke-Mikulicz pyloroplasties, because of the larger volume contained in the stomach at 15 min. 15-min glucose meal acid secretion correlated with basal acid concentration but not with insulin-stimulated gastric acid output. The small excess of acid in the Heineke-Mikulicz group's 15-min glucose meals may represent a small, maintained excess of gastric acid in this group detected only in the brief glucose meals due to rapid and erratic gastric emptying of liquids after vagotomy.     

Gastric acid secretory response in Helicobacter pylori-positive patients with duodenal ulcer disease.

BACKGROUND: Patients with duodenal ulcer (DU) have an increased parietal cell mass and sensitivity to secretagogues, with increased acid output. AIM: To determine the effect of Helicobacter pylori eradication on parietal cell sensitivity and gastric acid secretion. SUBJECTS AND METHODS: Twenty-five H pylori-positive DU patients and 18 H pylori-negative healthy volunteers were studied. Serum H pylori immunoglobulin G, basal acid output and acid secretory response to graded doses of pentagastrin were determined before and after treatment, at six months and at one year. Subjects were randomly assigned to ranitidine or sucralfate treatment for six weeks, and all DU patients received bismuth subsalicylate, metronidazole and tetracycline for the first two weeks. RESULTS: H pylori was eradicated in 66% of patients receiving sucralfate and 92% receiving ranitidine. Compared with healthy volunteers, DU patients demonstrated a 2.7-fold greater basal acid output, a 1.3-fold greater peak acid output, significantly higher acid output for each dose of pentagastrin and a 1.38-fold increase in the area under the pentagastrin dose acid response curve. Cure of H pylori, irrespective of ulcer healing regimen, resulted in a gradual decrease in acid secretory capacity with basal acid output, peak acid output and area under the pentagastrin dose acid response curve returning to healthy volunteer levels by one year. No demonstrable differences were observed in parietal cell sensitivity in all subjects before or after treatment. These data suggest that disturbances in acid secretion in H pylori-positive DU patients are not due to an increased parietal cell sensitivity to pentagastrin but rather due to an increased parietal cell mass with increased capacity to secrete acid, which gradually resolves following cure.     

Gastric secretory derangement in Menetrier's disease

Summary Two cases of Menetrier's disease with occult gastrointestinal albumin loss, absence of free hydrochloric acid, and increased uropepsinogen excretion are presented.The absence of free hydrochloric acid is explained by the combination of edema and inflammatory reaction interfering with passage of the hydrochloric acid into the gastric cavity and its neutralization by the increased amount of albumin exuded into the stomach.The decrease in gastric pepsinogen secretion associated with an increased uropepsinogen excretion is probably due to a derangement of the normal exocrine-endocrine partition.The study reported in this article was supported by a Graduate Training Grant in Gastroenterology 2A-5177, National Institutes of Health Grant O6-22 from USPHS, and a special research fund.We are indebted to Dr. Robert B. Burton, Department of Medicine, for making Case I available for this study and to Dr. Roger Terry for interpretation of the histologic specimens.     

Gastric secretory conditions and plasma gastrin levels in rats after prolonged treatment with cimetidine

Effects of 4 weeks of treatment with oral cimetidine, 100 mg/kg twice daily, on gastric secretion and plasma gastrin levels were studied in rats. Pylorus ligation-induced and pentagastrin-stimulated gastric secretions were little changed at days 1, 3, and 10 after cessation of cimetidine treatment as compared to the controls. Histamine-stimulated acid secretion was significantly higher in the cimetidine-treated group than in the controls at day 3 after cimetidine treatment but was unchanged at days 1 and 10. A single oral administration of cimetidine at 100 mg/kg significantly increased plasma gastrin levels 4 hr after the treatment in refed rats but not at 2 and 8 hr later. Plasma gastrin levels significantly decreased at days 3 and 10 after cessation of cimetidine treatment as compared to the controls. Thus, while prolonged treatment with cimetidine induces a transient increase in response of parietal cells to histamine and a reduction of food-stimulated gastrin release, it does not seem to induce other appreciable changes in gastric secretion.     

Gastric inflammation triggers hypersensitivity to acid in awake rats

BACKGROUND & AIMS: Changes in visceral sensation contribute to the development of dyspepsia. Nonhuman models have previously focused on responses to mechanical stimulation. We studied the response to acid stimulation in the normal and inflamed stomach in rats. METHODS: A balloon and gastrostomy catheter were implanted into the stomach. Electromyographic responses to gastric balloon distention or acid administration through the gastrostomy were recorded from the acromiotrapezius muscle. To characterize chemonociceptive pathways, 0.75 mL HCl (0.05-0.3 N) or saline were given intragastrically in controls and animals after vagotomy, splanchnic nerve resection, or chemical denervation with capsaicin. The effect of inflammation was examined after induction of mild diffuse gastritis using iodoacetamide or creating gastric ulcers by injecting 60% acetic acid for 45 seconds into a clamped area of the stomach. RESULTS: Visceromotor electromyographic responses increased within 2 minutes after HCl administration (0.15 and 0.3 mol/L) but not saline or lower acid concentrations. Vagotomy and pretreatment with capsaicin but not splanchnic nerve resection abolished this response. Prior acid administration did not acutely sensitize animals to subsequent gastric distention. Gastritis and gastric ulcers enhanced the visceromotor responses to intragastric acid. CONCLUSIONS: In awake rats, visceromotor responses to intragastric acid are quantifiable, reliable, and reproducible. Aversive responses to acute noxious chemical stimuli primarily require vagal but not spinal sensory pathways. Injury-induced sensitization to intragastric acid administration is consistent with a potential role of chemical stimulation in triggering dyspeptic symptoms.     

Gastric acid secretory responses to some purified foods and to additions of sucrose or olive oil

The total outputs of acid from vagally innervated pouches of 6 dogs in response to the ingestion of equicaloric meals of lean meat, purified proteins (lactalbumin, gluten, milk casein, and egg albumin), olive oil, and sucrose were determined. In comparison to the outputs to the meals of meat, equicaloric quantities of sucrose, methylcellulose (inert control meal), olive oil, and egg albumin produced the least acid; 25, 31, 40, and 42% of the meat response, respectively. The other purified proteins stimulated the production of acid equivalent to 60–92% of that obtained with meat. Except for egg albumin, the quantity of acid secreted in response to the ingestion of these foods was directly related to their buffering capacity.An additional study, involving 4 additional dogs with innervated pouches, was made of the effect of adding 100 calories of sucrose, olive oil, or meat to a meal of 100 calories of meat. The outputs obtained were 85, 85, and 87% of those calculated by summing the separate 100-calorie outputs of the meals or multiplying the 100-calorie output to meat by 2. Provision of one-half of the calories of a 200-caloric meal by fat did not produce a greater reduction of secretion from that expected than equcaloric quantities of sugar or meat.Supported in part by Research Grant G-6207 from the National Science Foundation, and in part fulfilled the requirements for the degree of Master of Science in Nutrition awarded to Camilla Kotrba, Graduate School, University of Minnesota, 1960.     

Gastric secretory studies in patients undergoing chronic hemodialysis

Summary The composition of gastric secretion in the presence of azotemia has been well defined. The composition of gastric secretion in patients undergoing chronic hemodialysis has not been previously studied. Several reports emanating from dialysis centers in both the United States and England suggest that peptic ulceration may occur more frequently in patients undergoing chronic hemodialysis than in the general population. To better understand the etiology of peptic disease and the possible relationship existing between it and gastric secretion in a chronically hemodialyzed population, gastric secretory studies were performed in a series of 11 patients. The results of these studies indicate basal hyposecretion and hypoacidity to be the most characteristic feature of this group. Following maximal Histalog stimulation, patients were able to secrete a normal amount of gastric juice with a normal pH. Of the patients studied, only one, who manifested basal hyperacidity, had peptic disease. Correlation between volume and acidity of gastric juice and age, duration and type of disease, and biochemical abnormalities could not be demonstrated. It is concluded that factors other than gastric acidity must be implicated in peptic disease occurring in a chronically hemodialyzed population.The authors wish to thank Dr. Robert A. Levine for his advice and criticism.     

Gastric histomorphology and secretory biochemistry after biliopancreatic diversion

When paired data are considered and unpaired results are compared with controls, it appears that no significant changes of gastric histomorphology occur following biliopancreatic diversion.     

Gastric mucosal blood flow and acid secretion in portal hypertensive rats

The purpose of this study was to examine gastric mucosal blood flow, measured by hydrogen gas clearance, and acid secretion in portal hypertensive rats. Chronic portal hypertension was induced by a two-stage complete portal vein occlusion procedure. Basal gastric mucosal blood flow was significantly higher in portal hypertensive rats than in sham-operated rats, but there was no difference in basal acid output. In response to administration of pentagastrin, there was the expected rise in both acid secretion and blood flow in sham-operated rats, but in portal hypertensive rats there was a significantly lower increase in acid output and no change in blood flow. In portal hypertensive rats pretreated with indomethacin to inhibit endogenous prostaglandin generation, both basal blood flow and acid secretion--and their response to pentagastrin administration--were the same as in non-indomethacin-treated sham-operated rats. We conclude that in portal hypertensive rats there is an increased gastric mucosal blood flow and an impaired acid output response to pentagastrin stimulation, and these changes appear to be mediated by an increase in endogenous prostaglandin.     

Gastric acid secretion and lesion formation in rats under water-immersion stress

In attempts to investigate the roles of acid in the pathogenesis of stress-induced gastric lesions, gastric acid secretion was studied in pylorus-ligated and lumen-perfused rats under restraint alone (R) or restraint with additional water immersion (WI). Gastric mucosal blood flow (GMBF) was measured with the aminopyrine clearance method in acute fistula rats. Acid secretion in pylorus-ligated rats significantly decreased under R or WI of either 3.5 or 7 hr stress. In the lumen-perfused or acute-fistula rats, exposure of rats to stress for 7 hr produced a similar decrease; however, in the WI group, there was a significant increase of acid secretion for 3-4 hr during stress, but not exceeding the prestress level. Only in the WI group did GMBF exhibit similar increases to those of acid secretory activity, and these increases were significantly inhibited by intraperitoneal administration of atropine (1 mg/kg) or cimetidine (60 mg/kg). Gastric lesions developed in both groups at 3.5 hr and became extensively severe at 7 hr only in the WI group. Cimetidine failed to influence the formation of lesions at 3.5 hr but significantly inhibited the later outgrowth of lesions at 7 hr, while atropine or pylorus ligation all but completely prevented lesions induced by either 3.5- or 7-hr WI stress. These results indicate that exposure of rats to stress (R or WI) generally decreased acid secretory activity, but there was a rise in acid secretion toward normal levels during WI stress, which may play an important role in the aggravating process of stress-induced gastric lesions.     

Gastric acid inhibits antral phase III activity in duodenal ulcer patients

Fourteen patients with duodenal ulcers and eight healthy volunteers were examined to measure interdigestive gastroduodenal motility and plasma motilin. In order to study the effects of gastric acid on the gastroduodenal motility, 20 mg of famotidine was administered intravenously. The motility index of the gastric antrum and the duodenum, as well as the pH in the duodenal bulb were calculated. The duodenal pH was significantly lower and the gastric motility index was significantly weaker before the duodenal interdigestive migrating complex (IMC) in the ulcer patients than in the controls. Motilin levels increased before the duodenal IMC and decreased afterwards in both groups. Famotidine significantly increased the duodenal pH and the gastric motility index before the IMC, but no changes in the motilin level were noted. We conclude that duodenal ulcer patients have duodenal hyperacidity that results from increased inflow from the antrum and antral hypomotility during the gastric IMC and that these changes are normalized by the administration of famotidine. These results suggest that gastric acid inhibits antral contraction during the gastric IMC.