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Results for “GASTRIC ACIDITY DETERMINATION”

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At least 415 records · Page 23Linked to original sources
PubMed1981

[Gastric acidity in a double ulcer (of the stomach and duodenum)].

Gastric salt-acid secretion was studied in three comparative patient groups with gastric ulcer, endoscopically confirmed, combination of gastric and duodenal ulcers. In the patients with double localization of the ulcer (stomach and duodenum) - hyperacidity was determined after pentagastrin stimulation. Acid-salt secretion was higher than that of the patients with gastric ulcer and was close to the secretion of those with duodenal ulcer, being but with a high standard deviation, necessitates consideration to be given to each concrete case of treatment. No discrepancy in the volume of gastric secretion before meals was established, thus impugning the role of pylor stasis in the genesis of secondary gastric ulceration. The incidence of atrophic gastritis in case of gastric and double ulcer is almost identical, hence attention is paid to the duodeno-gastric reflux as an eventual cause for damaging gastric mucosa with its successive ulceration in the patients with duodenal ulcer of many years. That is the reason, drugs enhancing the resistance of gastric mucosa as well as methoclopramid intake are proposed additionally to the drugs, neutralizing or blocking the gastric acid-salt secretion.

Adult↗
PubMed1995

Abnormal intestinal motor patterns explain enteric colonization with gram-negative bacilli in late radiation enteropathy.

BACKGROUND & AIMS: Bacterial overgrowth and intestinal pseudo-obstruction may succeed abdominal radiotherapy, and absence of intestinal migrating motor complex (MMC) has been reported in bacterial overgrowth. The aims of this study were to address the relationship between intestinal patterns of motility and gastrointestinal microflora and to elucidate the pathogenesis of late radiation enteropathy. METHODS: Forty-one consecutive female patients with symptoms of late radiation enteropathy were examined by prolonged ambulatory manometry, culture of gastric and duodenal samples with quantification of gram-negative bacilli (GNB) by the glucose gas test, the [14C]D-xylose breath test, and determination of pH and short-chain fatty acids in gastric juice. RESULTS: The intensity of MMC explained 61% (P < 0.001) and 71% (P < 0.001) of the variability of GNB in the stomach and duodenum, respectively, corresponding to the severity of disease. Abnormal MMC index and presence of irregular bursts were the best predictors of GNB (86%; P < 0.001, multiple regression). Fasting gastric pH explained gastric bacterial counts (63%; P < 0.001) but did not predict GNB. CONCLUSIONS: Impaired motility emerges as a causal factor for gastrointestinal colonization with GNB, whereas hypochlorhydria facilitates unspecific gastric colonization. Abnormal motility and GNB in the proximal small intestine are essential factors in the pathogenesis of severe late radiation enteropathy.

Adult↗
PubMed1995

Pathologic duodenogastric reflux associated with persistence of symptoms after cholecystectomy.

BACKGROUND: The aim of this study was to determine whether increased duodenogastric reflux contributes to postcholecystectomy symptoms. METHODS: Gastric pH monitoring, hepatobiliary scintigraphy, gastric emptying scans, and gastric acid analysis were performed in asymptomatic (n = 10) and in symptomatic (n = 27) patients after cholecystectomy. Normal subjects (n = 20), patients with dyspepsia related to gastric acid hypersecretion (n = 20), patients with reflux gastritis after gastric surgery (n = 10), and patients with confirmed primary pathologic duodenogastric reflux (n = 10) were studied as controls. Symptomatic patients also underwent upper gastrointestinal endoscopy. RESULTS: Symptomatic patients had significantly increased interprandial gastric exposure to pH < 3 compared with asymptomatic subjects, which correlated well with a high incidence of hepatobiliary scans positive for abnormal duodenogastric reflux and chronic gastritis on endoscopy. Gastric alkaline exposure in symptomatic patients was similar to that seen in patients with primary pathologic duodenogastric reflux and patients with duodenogastric reflux related to gastric surgery. Gastric acid secretion and gastric emptying were not altered. Five patients tested before and after laparoscopic cholecystectomy showed that nocturnal gastric alkalization was enhanced after operation. CONCLUSIONS: This study suggests that excessive duodenogastric reflux may be responsible for persistence of symptoms after cholecystectomy.

Adult↗
PubMed2003

Primary duodenogastric reflux in children and adolescents.

UNLABELLED: Primary duodenogastric reflux is a rare disorder in adults which has not yet been documented in children. Six young patients, aged 4.5 to 16.5 years (median 13.5 years) presented with atypical reflux symptoms persisting from 1 to 84 months (median 8 months) and unresponsive to classical antacid therapy. In all six patients, 24 h gastric bilimetry showed excessive bile exposures for absorbances ranging from 0.25 to 0.60. The fraction of time (supine period) above the 0.25 absorbance threshold ranged from 30% to 75% while the 95th percentile value for healthy adults is 31%. In all patients tested, hepato-iminodiacetic acid scintigraphy revealed the occurrence of a massive duodenogastric reflux and four out of five patients had an alkaline shift (fraction of time pH >8 on 24 h lower oesophageal pH monitoring) ranging from 4.2% to 20% (control values 0.0% to 2.9%). Endoscopic findings included abundant bilious gastric leak (6/6) and chronic prepyloric Helicobacter pylorinegative gastritis (2/6). Daily administration of cisapride, sucralfate with or without omeprazole resulted in an improvement of symptoms in five patients within 15 days. This treatment was ineffective in one patient who became symptom-free only after a surgical duodenal switch with fundoplication was performed. CONCLUSION: primary duodenogastric reflux is a rare foregut disorder of unknown origin occurring in late childhood. If suspected, 24 h intragastric bilimetry appears to be a useful investigation to confirm the diagnosis.

Adolescent↗
PubMed1993

Influence of gastric acidity on fluoride absorption in rats.

The rate of F absorption from the stomach is pH-dependent, with greater absorption at low pH. Since the rate of absorption is also strongly influenced by the rapidity of gastric emptying, we have compared the relative importance of gastric acidity and gastric emptying in overall F absorption. Male rats (350 g, n = 85) were pre-treated with cimetidine (to inhibit gastric acid secretion) or pentagastrin (to stimulate gastric acid secretion) or were untreated controls, and given 50 micrograms F by stomach intubation. The pH of the F-containing solution was varied in the cimetidine-pre-treated group (pH 1.5, 5.5, 8.5), and was 5.5 for the control and pentagastrin-pre-treated groups. Gastric emptying was measured by addition of 14C polyethylene glycol to the F solution as an unabsorbed marker of fluid movement. F absorption was measured after 10, 20, and 40 min. The rate of gastric emptying was unaffected by pre-treatment or pH of the intubating solution. Initially, F absorption was greatest at low pH. After 40 min, absorption was comparable in all groups, averaging approximately 70% of the initial dose. The extent of absorption from the stomach was inversely related to pH, but increased absorption from the small intestine compensated for the low gastric absorption at high pH.

Absorption↗
PubMed1975

The negative feedback mechanism of gastric acid secretion: Significance of acid in the gastric juice in man and dog.

As reported previously, gastrin-stimulated gastric secretion in the dog and in man was suppressed by an intravenous infusion of secretin, These results, both in the dog and in man, also were obtained by introduction of acid into the duodenum, which indicated that both endogenous and exogenous secretion inhibit gastrin-stimulated gastric secretion at the oxyntic cell level. Feeding a test meal in man gave rise to an increase of plasma gastrin, reaching a peak of 120 pg. per milliliter at 15 minutes after feeding and remaining above control level for 2 to 3 hours. Is was found that plasma gastrin was suppressed greatly during the intravenous infusion of pure secretin. In animal experiments endogenous gastrin release produced by irrigation of the antral pouch also inhibited both endogenous and exogenous secretin. These results indicate that secretin inhibits gastrin release at the G-cell level in the antrum. On the other hand, it also was observed that endogenous gastrin release ceased when the pH of the perfusate dropped below 2.5. The following conclusions are drawn from the above findings. (1) Gastrin release is suppressed primarily by direct contact of acid with the antrum. The feedback mechanism in this case operates intraluminally in the stomach. (2) The low pH content of the stomach stimulates the release of secretin from the duodenum. The secretin released in this way not only inhibits gastric acid secretion at the oxyntic cell secretin released in this way not only inhibits gastric acid secretion at the oxyntic cell secretin released of gastrin at the G-cell level in the antrum. The level but also blocks the release of gastrin at the G-cell level in the antrum. The feedback mechanism brought about by acid of gastric origin occurs through the general circulation.

Animals↗
PubMed2002

Prevention of HCl-ethanol induced gastric mucosal injury in rats by Garcinia cambogia extract and its possible mechanism of action.

Oral pretreatment of rats with G. cambogia fruit extract (1 g/kg body weight/day at interval of 7 and 15 days) protected gastric mucosa against HCl-ethanol induced damage by decreasing the volume and acidity of gastric juice. Increased lipid peroxidation, decreased activity of antioxidant enzymes, altered levels of protein and glycoproteins in the ulcerated mucosa, and gastric juice were maintained at near normal levels in G. cambogia pretreated rats. The results suggest the anti-ulcer activity of G. cambogia by virtue of its ability to decrease acidity and increase mucosal defense.

Animals↗