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At least 523 records · Page 29Linked to original sources
PubMed1985

[Bacterial colonization of the stomach caused by acid neutralization and inhibition of stomach emptying].

Gastric bacterial overgrowth was studied in 8 healthy volunteers. Total bacterial counts, nitrate-reducing bacteria and nitrite concentration were determined in fasting gastric juice before and after 4 weeks of treatment with a strong or with a mild antacid drug, a placebo preparation and the spasmolytic agent papaverine which is known to inhibit gastric evacuation. Placebo therapy and the mild antacid did not change any of the above parameters studied. The strong antacid caused a significant increase in the pH of gastric contents which was accompanied by an enormous increase in total bacterial counts, nitrate-reducing bacteria and nitrite concentration. Papaverine which did not cause a significant elevation of pH also definitely increased bacterial counts and nitrite concentration of gastric juice. Four weeks following termination of each treatment procedure, however, all changes outlined above had returned to pretreatment values. These results indicate that reversible gastric bacterial overgrowth under therapeutical conditions may occur when acidity of the stomach is reduced or gastric evacuation is retarded.

Adult↗
PubMed1987

Prevention of aspirin-induced gastric mucosal injury by histamine H2 receptor antagonists: a crossover endoscopic and intragastric pH study in the dog.

Histamine H2 receptor antagonists have been reported to protect the gastric mucosa of animals and humans against aspirin-induced damage. It is unclear, however, whether this protective effect can be observed at doses less than those needed to markedly inhibit gastric acid secretion. We have developed a single-dose endoscopic assay system of aspirin-induced gastric mucosal injury in normal conscious dogs. In this model, severe gastric mucosal injury and a decrease in the pH of the gastric luminal contents were consistently demonstrated 2 h after the oral administration of 100 mg/kg of aspirin. Pretreatment with three histamine H2 receptor antagonists (cimetidine, ranitidine, BMY-25271), prevented both of these effects in a dose-related manner. All three H2 receptor antagonists reduced gastric mucosal injury only at doses that were greater than those required to prevent the aspirin-induced decrease in gastric luminal pH or to inhibit histamine-stimulated gastric acid secretion in Heidenhain pouch dogs. Plasma levels of aspirin were not altered by histamine H2 receptor antagonism. These results indicate that acid inhibition is an important component of the mechanisms whereby histamine H2 receptor antagonists protect the gastric mucosa from aspirin-induced damage in the dog.

Animals↗
PubMed1984

The relationship between gastric carcinoma and gastric juice lactate (L + D) and lactate dehydrogenase.

L-Lactate, D-lactate, and lactate dehydrogenase (LDH) levels were measured in the resting gastric juice of 73 patients and mean levels were found to be significantly higher in patients with gastric carcinoma than in those with benign gastric ulcer or those with normal stomachs. Raised levels of gastric juice L-lactate (greater than 1.3 mmol/l), D-lactate (greater than 0.15 mmol/l), and LDH (greater than 55 IU/1) were seen in 14 of 27 patients with carcinomas, two of 15 with benign ulcers, and six of 31 controls. Both L/D-lactate and LDH levels correlated with tumor size and depth of invasion. While six problem cases with large gastric lesions were correctly diagnosed using these indices, there was only poor sensitivity and moderate specificity, as early cancers had normal L/D-lactate and LDH levels, and these indices were raised in a significant number of controls. Thus while it is of interest that L/D-lactate and LDH are elevated in the gastric juice of patients with gastric carcinoma there appears to be little optimism for using these indices in the early diagnosis of gastric neoplasia.

Adult↗
PubMed2003

Intrapharyngeal distribution of gastric acid refluxate.

OBJECTIVES/HYPOTHESIS: Determination of intrapharyngeal distribution of gastric acid refluxate is needed to better understand the pathogenesis of reflux-attributed aerodigestive tract disorders. The aims of the study were to determine intrapharyngeal distribution of gastric acid refluxate and to determine whether this distribution can better differentiate patients from control subjects compared with data obtained from a single hypopharyngeal site. METHODS: We prospectively studied 10 healthy volunteers, 12 patients with reflux laryngitis, and 15 patients with vasomotor rhinitis using a concurrent dual pharyngeal/dual esophageal pH recording technique. We determined the hypopharyngeal and oropharyngeal pH profile, including number, duration, and distribution of reflux events irrespective of and in correlation with intraesophageal pH profile using four different pH thresholds. RESULTS: Few drops in pharyngeal pH were found to be true reflux events based on their correlation with esophageal pH events. For the pharyngeal pH threshold criterion of a drop to 4.0 or less, 6 of 12 patients with reflux laryngitis, 5 of 15 patients with vasomotor rhinitis, and 2 of 10 normal control subjects exhibited a total of 25 (range, 1-5) distal pharyngeal acid reflux events. Overall, 34% of these events reached the oropharyngeal pH recording site. Between-group comparison for all levels of pH threshold criteria did not show any significant difference of reflux parameters in the hypopharyngeal or in the oropharyngeal sites among the studied groups. CONCLUSIONS: Reflux of gastric acid into the pharynx may extend to the region of the oropharynx in both patients and control subjects. Overall distribution of acid refluxate to the oropharynx is low but as groups is similar between healthy individuals and patients with reflux laryngitis and those with vasomotor rhinitis. Parameters of oropharyngeal acid reflux such as number and duration do not differentiate patients from control subjects.

Gastric Acid↗
PubMed1975

Gastric function in chronic renal failure. Effects of maintenance haemodialysis.

40 patients with chronic renal failure have been studied in order to determine why some patients with azotaemia have previously been reported to secrete abnormally large amounts of acid and some to secrete very little. 15 of the 40 patients were undergoing regular haemodialysis, while the remaining 25 patients had not been so treated. 10 of the 25 non-dialysed patients had much-impaired capacity to secrete acid. The impaired gastric secretory capacity was corrected and became abnormally great after some months of regular haemodialysis in 4 patients. Regular haemodialysis, by removing factors responsible for the gastric mucosal damage, permits manifestations of an underlying gastric hypersecretory state.

Creatinine↗
PubMed2004

Pentagastrin-induced gastric acid secretion in the diabetic rats: role of insulin.

Streptozotocin-induced diabetic rats have excessively pentagastrin-simulated acid output in which insulin seems to attenuate rather than further stimulate acid output. The aim of this study was to determine the insulin impact on pentagastrin-stimulated acid output of diabetic and non-diabetic rats to resolve whether an attenuated effect does exist. Diabetic rats were induced by the streptozotocin i.v. injection four days before acid study. Some streptozotocin-treated rats additionally received daily insulin (2.4 IU/kg) injection. Using an autotitrator, acid output was measured every five minutes by the titration of gastric perfusate. Basal output was collected for 45 min before the 90-min pentagastrin infusion (0.89 microg/kg/min). Plasma gastric inhibitory polypeptide (GIP) levels were measured. Both doses (0.067 and 0.133 IU/kg/min) of insulin infusion resulted in stimulated acid output in normal rats. The subsequent insulin infusion (0.133 IU/kg/min) for non-diabetic rats undergoing pentagastrin-treatment suppressed their stimulated acid output almost down to the basal level. Pentagastrin-stimulation led to the excessively increased acid output of diabetic rats throughout the whole infusion period (P < 0.01). Correction of hyperglycemia with insulin for diabetic rats normalized the stimulated acid output. Measured basal and stimulated plasma GIP levels of those diabetic rats during acid stimulation remained higher, regardless of insulin treatment (P < 0.05). Our results suggest that insulin has the ability to attenuate pentagastrin-stimulated acid output in rats, whereas GIP is not involved in this attenuation. This effect appears to be responsible for the excessive acid output of diabetic rats undergoing pentagastrin stimulation.

Animals↗
PubMed1981

Abnormal gastric emptying response to pentagastrin in duodenal ulcer disease.

The effect of pentagastrin on gastric emptying in duodenal ulcer disease (DU) is unknown. The evaluation of this effect is complicated by the simultaneous action of the hormone on gastric secretion. We compared gastric emptying and net gastric output in 17 patients with active DU to that of 11 healthy controls. A dye-dilution technique was used to determine net acid output, fractional emptying rate, and acid emptying rate during a basal period and after pentagastrin (6 microgram/kg/hr, intravenously). Net basal acid output observed in controls (54 +/- 10 microEq/min; mean +/- SE) was used as the primary criterion for separating DU patients into 12 normosecretor (30 +/- 10 microEq/min) and 5 hypersecretor patient groups (163 +/- 40 microEq/min). The pentagastrin-stimulated net acid output was significantly greater in hypersecretor patients than in controls (P less than 0.01) but was normal in normosecretor patients. Basal fractional emptying and acid emptying rates were significantly greater in hypersecretors than in controls (P less than 0.05) but were normal in normosecretors. In contrast, both normo- and hypersecretor patients had significantly greater fractional emptying (P less than 0.01) and acid emptying rates than controls (P less than 0.05) during pentagastrin infusion. Thus, a greater load of acid transiently enters the duodenum in duodenal ulcer disease following pentagastrin stimulation, even in the absence of gastric hypersecretion.

Adult↗