Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0847097 (acidity)
 15,165 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The neutralization of acid introduced into the duodenum has been found to be less intensive in patients with duodenal ulcer than in controls. The present work studied the possibility that chronic gastric hypersecretion injures the duodenal mucosa and thereby influences the neutralization system. Gastric hypersecretion was provoked for 3 weeks in 3 dogs by a daily injection of a gastrin preparation with prolonged effect. After a subcutaneous injection of this preparation given together with a test meal the acidity of both gastric and duodenal contents was found to increase significantly. After the 3 weeks of gastric hypersecretion the pancreatic bicarbonate response to exogenous secretin was unchanged, while the bicarbonate response to duodenal acidification was decreased from 2.03 mEq/30 min to 1.27 mEq/30 min (p less than 0.05), compatible with an impaired secretin release. Also the concentration of lactase, maltase, sucrase, and alkaline phosphatase in mucosal biopsies from the second part of the duodenum was significantly reduced (p less than 0.001). These results indicate that gastric hypersecretion causes mucosal damage in the duodenum and thereby reduces the release of secretin.
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PMID:Effect of gastric hypersecretion on the canine duodenum. 1 Jun 21

The influence of severe exocrine pancreatic disease on the acid-neutralizing capacity of the duodenum was studied in five patients with pancreatic insufficiency (PI) and six control subjects using duodenal perfusion-marker technique. Hydrochloric acid (0.1 N containing 1% PEG) was infused at constant rates (1.2, 4.5 and 7.0 ml/min) into the duodenum just distal to the duodenal bulb. Samples were aspirated from the tip of the duodenal perfusion tube located at the ligament of Treitz. All samples were analyzed for volume, pH, titrable acidity, PEG and [14C]PEG (gastric marker) determination. Patients with PI demonstrated significantly diminished ability to neutralize various acid loads as compared to controls who virtually completely neutralized acid loads in the range of maximal gastric acid secretion. Exogenous secretin did not significantly improve percent acid neutralized in PI. These data clearly indicate that patients with PI have significantly impaired ability to neutralize even small loads of acid in the duodenum.
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PMID:Impaired acid neutralization in the duodenum in pancreatic insufficiency. 3 15

The effect of Jorpes secretin on the urinary volume, pH, and excretion of sodium, potassium, chloride, bicarbonate, titratable acidity, ammonia and phosphate was studied in five healthy male volunteers with and without simultaneous aspiration of duodenal fluids. A three- to fourfold increase in urinary volume and sodium excretion occurred within the first 30 min after secretin injection and this was accompanied by a significant rise in urinary pH in each instance. Urinary bicarbonate excretion increased from 55 plus or minus 13 to 395 plus or minus 33 mueq/30 min after secretin injection. Aspiration of alkaline duodenal contents was accompanied by an even greater postsecretin increase in urinary bicarbonate excretion. No significant changes in arterial pH or blood gases were detected throughout the study. These observations are compatible with a direct effect of secretin upon the renal tubular reabsorption of water, bicarbonate, and other ions, and could account for the transient alterations in urinary pH occurring in response to a meal.
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PMID:Renal response to secretin. 23 65

Thirty patients with bile reflux gastritis, proven by gastroscopy and Milk 99mTc-EHIDA Test, were studied and their clinical features were compared with those of patients with non-bile reflux gastritis. The symptoms were similar in both groups of patients, whereas histologically in bile reflux gastritis there were more hyperemia of mucosa, more obvious edema in lamina propria and more polymorphonuclear infiltration. Furthermore, in bile reflux gastritis the histological changes were more severe in the antrum and decreased in severity toward the cardia. Acid secretion was significantly lower in patients with bile reflux gastritis than in patients with non-bile reflux gastritis while the serum gastrin level was significantly higher in the former than in the latter group. The authors suggest that there may be a vicious cycle among duodenogastric reflux, low level of gastric acidity and high level of serum gastrin. When duodenogastric reflux occurs, not only the bile salts damage the gastric mucosa and subsequently cause the back diffusion of hydrogen ion but also the alkaline duodenal juice neutralizes the gastric acid, resulting in decrease of gastric acidity. The bile salts and low acidity can stimulate the release of serum gastrin which antagonizes the effects of cholecystokinin and secretin on pyloric tone and aggravates the duodenogastric reflux.
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PMID:[Clinical characteristics of bile reflux gastritis]. 273 41

Renal gastrinoma has not been previously reported. A 12-year-old boy with Zollinger-Ellison syndrome was found to have a renal tumor. No other tumor was detectable by imaging techniques, and selective venous sampling for gastrin showed a significant renal vein to vena cava gradient. Nephrectomy was performed, and examination of the tumor showed typical histologic features of an endocrine tumor. G cells were apparent by electron microscopy, and immunoperoxidase staining for gastrin, neuron-specific enolase, and chromogranin were positive. The gastrin content was unusually low for gastrinomas: 128 pg/g. Following nephrectomy, fasting gastrin and secretin stimulation testing were normal. Basal acidity was reduced by 60% but remained elevated at 39 mmol H +/h (hydrogen ion per hour). We speculate that renal gastrinoma may be characterized by uniquely poor gastrin storage and that curative resection of all gastrinoma tissue may not necessarily be associated with immediate complete suppression of hyperacidity.
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PMID:Zollinger-Ellison syndrome associated with a renal gastrinoma in a child. 287 87

In 27 infants aged 20 to 65 days with clinically and roentgenologically proved hypertrophic pyloric stenosis gastric juice analyses were performed according to Lambling. Basic acid output and maximal acid output in these infants were significantly increased as compared to healthy infants of the same age group. The higher acid output in the hypertrophic pyloric stenosis group was due to higher volumes and a higher acidity of the gastric juices. Basic acid output and maximal acid output increased following pylorotomy. There is evidence, that hyperacidity in pylorus stenosis of infancy is primarily and not due to the pyloric constriction. There was a distinct correlation between the degree of metabolic alkalosis and diminished acid outputs. The findings support the thesis, that infantile hypertrophic stenosis is originated by an increased parietal cell mass. The increased acid secretion and the enhanced release of secretin and cholecystokinin are supposed to originate the hypertrophy of the pyloric muscle.
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PMID:[Results of Lambling gastric juice analysis in infants with spastic hypertrophic pyloric stenosis (SHPS)]. 373 14

The effect of duodenal acidification on pentagastrin-stimulated gastric acid secretion was studied in 43 duodenal ulcer patients and in 17 normal controls. Three types of responses were observed: group A, no inhibition of gastric acid secretion occurred in 17 (40%) ulcer patients and in three (18%) controls (p less than 0.05); group B, inhibition of gastric acidity occurred in seven (16%) ulcer patients and in 12 (71%) controls (p less than 0.05), and group C, retarded gastric acid inhibition occurred in 19 (44%) duodenal ulcer patients and in 2 (12%) controls (p less than 0.05). Secretin levels did not increase after duodenal acidification, the higher percentages of failure being observed in groups A and C (p less than 0.05). The pH of the duodenal aspirate was 4.9 +/- 2 and 7.7 +/- 1.4 in ulcer patients and controls, respectively (p less than 0.05), with the low levels being detected in groups A and C (4.7 +/- 2 and 5.3 +/- 2.1) compared to group B (7.3 +/- 1.7; p less than 0.05). The results show that responses of duodenal ulcer patients to duodenal acidification are heterogeneous, and that failure of gastric secretion inhibition and defective intraduodenal acid neutralization are related.
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PMID:Physiopathological heterogeneity of the duodenal mechanisms that inhibit gastric acid secretion in duodenal ulcer patients. 403 45

Serum gastrin levels in patients with pernicious anaemia were measured by immunoassay in the fasting state, following gastric perfusion with 0.9% saline, 0.1N hydrochloric acid, and solutions of increasing acidity, and after the intravenous injection or infusion of secretin. The fasting serum gastrin level was measured in 21 patients with pernicious anaemia and found to be elevated at 1,036 +/- 215 pg per ml. Gastric perfusion with saline (pH 4.7) caused a mean fall in serum gastrin of 30% in four patients; perfusion with hydrochloric acid caused a further slight fall. Perfusion with solutions of increasing acidity resulted in a sharp fall in serum gastrin levels when the acidity was changed from pH 6 to pH 4. A single intravenous injection of secretin produced a mean maximal fall of 44% in the serum gastrin level in four patients, whereas continuous infusion of secretin produced a fall of 35% in four other patients. These studies suggest that the gastrin-secreting cells of the stomach are not affected by the atrophic process in pernicious anaemia and remain subject to the regulating control of acid and secretin.
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PMID:Radioimmunoassay of gastrin: studies in pernicious anaemia. 554 65

In the fasting state, the secretions of isolated total gastric pouches were higher than what was found in classical gastric fistulae. Serum gastrin was lower in operated rats than in normal non-operated rats. The proximal duodenum would contain a substance which inhibited volume and acidity secretion and stimulated pepsin secretion. This role could be developed upon secretin and its family present in high concentration in the upper duodenum. If the vagus was necessary to volume and acid secretion, its action on pepsin secretion was strengthened by the proximal duodenum. After an intestinal meal, all secretions were enhanced, confirming the hypothesis that the intestine would contain an hormone which would act through the vagus, principally for volume and acid secretions and partially for pepsin secretion.
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PMID:Secretions of isolated total gastric pouches in fasting and fed rats. 680 Aug 37

To ascertain whether any of the well-known effects of intravenous ethanol on pancreatic and gastric secretion could be due to its metabolite--acetaldehyde, a strong cytotoxic and sympathomimetic agent--acetaldehyde was given intravenously for 1 h (50, 100, and 200 mg/kg/h) in seven dogs. Acetaldehyde did not modify pancreatic secretion stimulated with secretin and caerulein, but under basal conditions 200 mg/kg/h slightly increased the volume and protein content of pancreatic juice. Acetaldehyde increased gastric secretion up to 4.03 meq/15 min in a dose-dependent manner, while serum gastrin remained unchanged. The increase of acidity persisted after propranolol and was inhibited but not abolished by ganglionic blockade. It can be concluded that physiological concentrations of acetaldehyde do not interfere with pancreatic secretion and that it is possible that the stimulatory effect of ethanol on gastric secretion is mediated at least partly through acetaldehyde.
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PMID:The effect of acetaldehyde on pancreatic and gastric secretion. 720 90


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