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At least 559 records · Page 31Linked to original sources
PubMed1987

Mechanism of release of gastric luminal somatostatin-like immunoreactivity in response to pentagastrin and sham feeding in man.

We studied in five healthy volunteers whether the cholinergic pathway regulated the secretion of gastric intraluminal somatostatin-like immunoreactivity (SLI) in response to stimuli of pentagastrin infusion (0.9 micrograms/kg/h, intravenously) and sham feeding. We measured gastric secretory volume, hydrogen ion output, and SLI at base line, during pentagastrin infusion, after sham feeding, and after applications of atropine (0.0, 0.7, 7.0 micrograms/kg, intramuscularly) given before pentagastrin and sham feeding. The stimuli were given randomly, at separate times on different days. After each stimulus, eight 15-min gastric juice collections were made; samples were adjusted to pH 7, pepstatin-A and aprotinin were added, and samples were extracted with acetone to determine SLI by radioimmunoassay. Pentagastrin and sham feeding significantly increased gastric luminal SLI secretion, which appeared to correlate with the increases in volume and acid output. Atropine at 7 micrograms/kg significantly suppressed gastric volume, acid, and SLI outputs stimulated by sham feeding; however, responses to pentagastrin stimulation remained unchanged. To conclude, the cholinergic mechanism regulates gastric intraluminal SLI response to sham feeding but not to pentagastrin infusion.

Adult↗
PubMed1992

[Gastric secretion of pepsin in gastroesophageal reflux complicated or not with peptic esophagitis].

Few data have concerned gastric peptic activity in reflux esophagitis. Gastric basal and pentagastrin-stimulated acid, pepsin, sialic acid (marker of gastric mucus erosion) and choline (marker of duodenal refluxate) outputs were measured in 75 patients with gastroesophageal reflux. Fifty-one patients had erosive esophagitis (grade greater than or equal to II) and 24 had no esophagitis or esophagitis grade I. In 12 patients of each group, gastric secretory parameters were correlated with results of 24-hour esophageal pH-metry. Stimulated pepsin output was significantly higher in patients with esophagitis than in the others (P less than 0.001). Basal pepsin output was significantly higher in women with esophagitis than in women without esophagitis (P less than 0.05). Acid, sialic acid, and choline outputs did not differ between the two groups. Thirty-seven and 49 percent of patients with esophagitis had elevated basal and stimulated pepsin outputs, respectively, as compared with 33 and 29 percent of patients without esophagitis. Thirty-one percent of patients with esophagitis had gastric acid hypersecretion, as compared with 25 percent of patients without esophagitis. There was no correlation between gastric secretory parameters and data obtained from esophageal pH-metry. Nevertheless, esophageal acid exposure was higher in patients with esophagitis than in patients without esophagitis. These results suggest that gastric proteolytic content is a pathophysiological factor for erosive esophagitis.

Adult↗
PubMed1991

[Changes in gastric secretory function in peptic ulcer patients after gastric resection].

Gastric function was studied in 69 peptic ulcer patients in the long-term period after gastric resection according to Billroth-I and Billroth-II. Enzyme-producing function of the stomach was appraised according to the blood pepsinogen content, acid-forming function was assessed with the aid of intragastric pH-metry, and mucus-forming one in accordance with the content of hexosamines and sialic acids in gastric juice. The patients showed different alterations in gastric function. A correlation analysis was used to establish the role played by the neurohormonal systems (leu-enkephalin, beta-endorphin, gastrin, somatotropin, triiodothyronine, thyroxine, cortisol) in the derangement of secretory function of the resected stomach. The data obtained enable one to come closer to understanding the ineffectiveness in some cases of drug and surgical therapy of peptic ulcer. On the other hand, specification of the regularities of the impairment of secretory function of the stomach will be helpful in elaborating methods of gastric function correction at the neurohormonal level.

Adult↗
PubMed2003

Lung transplantation exacerbates gastroesophageal reflux disease.

INTRODUCTION: A high prevalence of gastroesophageal reflux (GER) has been reported in lung transplant recipients and is possibly linked to the development of bronchiolitis obliterans syndrome. The etiology of posttransplant GER remains unknown but may occur due to the transplant operation or posttransplant medications, or represent preexisting GER disease. We evaluated these possibilities by studying the nature and severity of GER in a cohort of patients before and after lung transplantation. METHODS: Total, upright, and supine acid contact times were recorded in lung transplant recipients who underwent 24-h pH studies before and after transplantation. Patients also underwent esophageal manometry and gastric-emptying studies. Medications for acid suppression and gastric motility were discontinued before testing. Paired comparison between pretransplant and posttransplant results was performed using a paired t test. RESULTS: Twenty-three patients were included in the analysis. The mean age was 51.5 years, and native diseases included emphysema (n = 11), cystic fibrosis (n = 4), pulmonary fibrosis (n = 3), and others (n = 5). Posttransplant studies occurred a median of 100 days after transplantation. After lung transplantation, the total acid contact time increased a mean of 3.7% (p = 0.03) and the supine acid contact time increased a mean of 6.4% (p = 0.019). Thirty-five percent (8 of 23 patients) had abnormal acid contact times before transplant, and 65% (15 of 23 patients) had abnormal acid contact after transplant. Changes in acid contact times were not explained by changes in esophageal or gastric motility. Only 20% (3 of 15 patients) with abnormal posttransplant pH studies were symptomatic. CONCLUSIONS: There is a significant increase in GER after lung transplantation, as measured objectively by 24-h pH studies, despite a lack of symptoms in most patients. Further research is needed to determine the physiologic mechanisms of posttransplant GER and its impact on long-term allograft function.

Esophagus↗
PubMed1989

Proline is not useful as a chemical probe to measure nitrosation in the gastrointestinal tract of patients with gastric disorders characterised by anacidic conditions.

Aspirated fasting gastric juice from patients with lesions of the gastrointestinal tract and from healthy controls was analysed for nitrite before and after (30, 90, and 240 min) oral administration of 200 mg nitrate. Wilcoxon's rank-sum tests showed no significant differences in fasting gastric juice nitrite concentrations between healthy controls and patients after proximal gastral vagotomy or with gastric/duodenal ulcer (median less than or equal to 0.7 ppm NO-2) and only moderate increases after nitrate administration. Chronic atrophic gastritis patients and patients with Billroth I or II gastric resections showed median concentrations of 2 ppm NO-2 which increased to 20 ppm (up to 200 ppm in one Billroth II patient) after administration of nitrate. Endogenous formation of N-nitrosoproline using the NPRO-test was determined in two groups with low (healthy control and proximal gastral vagotomy patients) and high (Billroth I and II patients) gastric nitrite concentrations. After 12 h fasting, 200 mg nitrate was orally administered, followed 30 min later by 500 mg L-proline. Endogenously formed N-nitrosoproline which is quantitatively excreted in urine was determined in urine over the following 24 hours. In over 80% of the urine samples collected from Billroth I and II patients no detectable NPRO was found whilst in over 85% of the healthy controls and proximal gastral vagotomy patients up to 33.5 micrograms NPRO was detected. In vitro nitrosation kinetics showed that at gastric pH greater than 4 present in both, patients with Billroth I and II resections and with chronic atrophic gastritis, nitrosation of proline does not occur. As alternative chemical probes for quantifying potential endogenous nitrosation in hypoacidic patients the methyl and ethyl esters of proline were investigated. In vivo nitrosation of these two new probes was established in animal experiments using rats and was shown to occur in vitro at pH 4-5. During incubation in human gastric juice, however, almost 30% ester cleavage by non-specific gastric esterases occurred within the first five minutes, thus further limiting the use of these compounds in determining endogenous nitrosation in hypoacidic patients.

Gastric Acidity Determination↗
PubMed1994

Effect of ranitidine on basal and bicarbonate enhanced intragastric PCO2: a tonometric study.

A high intragastric PCO2 (iPCO2), determined tonometrically, is the main factor participating in a low gastric intramucosal pH (pHi) and may point to gastric mucosal ischaemia. iPCO2 might also increase, however, after buffering of gastric acid by bicarbonate; the magnitude of this effect and the efficacy of H2 blockers to prevent it are unclear. Ten healthy volunteers (20-24 years) were studied at baseline and after oral ingestion of 500 mg sodium bicarbonate. The same test was carried out one hour after intravenous injection of 100 mg ranitidine. A glass pH electrode for continuous gastric juice pH measurements and a Tonomitor catheter were placed 10 cm distally from the gastro-oesophageal junction. iPCO2 was measured in saline boluses, infused at 30 minute intervals in the balloon at the tip of the Tonomitor. Before ranitidine was given, basal iPCO2 (mean (SD)) was 8.40 (2.53) kPa, and increased to 19.20 (5.87) kPa after sodium bicarbonate (p < 0.001). After ranitidine, the gastric juice pH increased from 1.8 (0.9) to 5.6 (1.3) (p < 0.05), while basal iPCO2 was 5.60 (0.67) kPa (p < 0.01) and did not change after sodium bicarbonate (6.27 (2.67) kPa)). iPCO2 values after acid secretion suppression were similar to those in capillary blood (5.60 (0.40 kPa)). The difference between intragastric and blood PCO2 during normal acid secretion probably results from buffering of gastric acid by gastric bicarbonate, rather than by duodenogastric reflux or saliva entering the stomach. During acid secretion suppression, intragastric equals blood PCO2, even after oral ingestion of sodium bicarbonate. Hence, acid secretion inhibition is mandatory for proper assessment of iPCO2 and pHi as specific measures of the adequacy of gastric mucosal blood flow.

Adult↗