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PubMedDate not supplied

Acid-related diseases following retrosternal stomach interposition.

BACKGROUND/AIMS: Esophagectomy and reconstruction with retrosternal stomach interposition implies bilateral truncal vagotomy, which supposedly causes gastric functional impairment. METHODOLOGY: Esophagectomy and reconstruction with retrosternal stomach interposition was performed on 15 men (mean age: 58.4 years) and 3 women (mean age: 43.6 years). The stomach was pedicled on the right gastric and right gastroepiploic artery without performing pyloroplasty. The cervical side-to-end anastomosis was sutured manually. The functional results were assessed 2-4 years postoperatively, by determining 24-hour qualitative intragastric pH-measurement, fluoroscopical gastric emptying studies, fasting gastrin levels, and endoscopy with biopsy studies. RESULTS: Endoscopy and biopsy confirmed esophagitis in 12 patients, gastritis in 15 and a gastric ulcer in 1 case. Fluoroscopic examination documented a normal passage of contrast medium in 17, slight impairment in 1 case treated by balloon dilatation of the pylorus. Qualitative intragastric pH-measurement revealed a total pH < 3 in 22.5-98.05% of measuring events (mean: 74.31%) within 24 hours, in 18 cases. Only 4 patients had pH < 3 in less than 50%. Fasting gastrin levels (normal range: 25-110 mU/L) varied from 48.78 mU/L-168.20 (mean: 85.23 mU/L). Only 3 patients had levels > 110 mU/L (maximum: 168.20 mU/L). CONCLUSIONS: Acid-related diseases may also occur after truncal vagotomy and retrosternal stomach interposition. Routine follow-up endoscopy and biopsy studies should be done to prevent inflammatory complications and maintain the patient's quality of life.

Adult↗
PubMedDate not supplied

Diflunisal disposition. Role of gastric absorption in the development of mucosal damage and anti-inflammatory potency in rodents.

Aspirin shows a high incidence of gastric side effects. These are thought to result from both systemic and local effects during drug absorption. In contrast, a lipophilic derivative of salicylic acid, diflunisal, causes significantly fewer adverse gastric effects. This is thought to be due to a lack of gastric absorption. To test this hypothesis, three types of experiments were performed with diflunisal: 1. Transgastric permeation was quantified under different pH conditions, using an isolated mouse stomach model. 2. Ulcerogenic potencies of buffered and unbuffered drug solutions were determined in rats. 3. The time course of its anti-inflammatory effect and the serum concentrations of diflunisal, given alone and with neutralizing buffer, were measured in rats with carrageenan-induced paw edema. Corresponding to the low gastric ulcerogenicity, absorption of diflunisal in the isolated stomach preparations was very small. However, absorption was pH-dependent and ranged between 0.69 and 8.73% with a maximum at pH 4.5. Gastric lesions were found to be more evident 24 hr after drug administration than after 5 hr. Comparing buffered vs. unbuffered diflunisal preparations, no difference in ulcerogenicity was detectable. However, using a buffered preparation, the anti-inflammatory effect of diflunisal was enhanced significantly (p less than 0.01), and elevated serum concentrations were found (p less than 0.05). The results show that raising the solubility of diflunisal does not influence gastric absorption or gastric toxicity considerably. However, its serum concentrations and systemic anti-inflammatory effects were significantly enhanced.

Absorption↗
PubMed1995

Effect of omeprazole on concentrations of clarithromycin in plasma and gastric tissue at steady state.

This study was conducted to determine (i) the effect of omeprazole on steady-state concentrations of clarithromycin and 14-(R)-hydroxyclarithromycin in plasma and gastric mucosa, (ii) the effect of clarithromycin on steady-state concentrations of omeprazole in plasma, and (iii) the effect of clarithromycin on the suppression of gastric acid secretion by omeprazole. Twenty healthy, Helicobacter pylori-negative male subjects completed this three-period, double-blind, randomized crossover study. In period 1, all subjects received 40 mg of omeprazole each morning for 6 days. Twenty-four-hour gastric pH monitoring took place on days -1 and 6. Pharmacokinetic sampling took place on day 6. In periods 2 and 3, subjects were randomly assigned to receive either 40 mg of omeprazole or omeprazole placebo daily for 6 days plus clarithromycin (500 mg) every 8 h for 5 days with a single 500-mg dose on day 6. Gastric tissue and mucus samples were obtained via endoscopy on day 5. Gastric pH monitoring and pharmacokinetic sampling took place on day 6. Two-week washout intervals separated the three study periods. Clarithromycin increased mean omeprazole area under the concentration-time curve from 0 to 24 h from 3.3 +/- 2.0 to 6.3 +/- 4.5 micrograms.h/ml (P < 0.05) and harmonic mean half-life from 1.2 to 1.6 h (P < 0.05) but did not significantly alter the effect of omeprazole on gastric pH. Mean clarithromycin area under the concentration-time curve from 0 to 8 h increased from 22.9 +/- 5.5 (placebo) to 26.4 +/- 5.7 micrograms.h/ml (omeprazole) (P < 0.05) when clarithromycin was administered with omeprazole. Analysis of variance revealed that mean concentrations of clarithromycin in tissue and mucus were statistically significantly higher when clarithromycin was given with omeprazole than when clarithromycin was given with placebo (P <0.001). Mean maximum observed concentrations of clarithromycin in the gastric fundus increased from 20.8 +/- 7.6 (placebo) to 24.3 +/- 6.4 micrograms/g (omeprazole), and those in the gastric mucous from 4.2 +/- 7.7 placebo to 39.3 +/- 32.8 micrograms/g (omeprazole). Similar increases were observed for the 14-(R)-hydroxyclarithromycin. These results show that omeprazole increases concentrations of clarithromycin in gastric tissue and mucus and may provide a mechanism for synergy between clarithromycin ad omeprazole that explains the excellent eradication of H. pylori seen in clinical trials.

Adolescent↗
PubMed1991

The effects of sucralfate and luminal stasis on recovery of the chambered rat gastric mucosa from taurocholate-induced damage.

We have previously shown, using a gastric chamber model, that both sucralfate and luminal stasis protected the rat gastric mucosa against the development of hemorrhagic erosions produced by subsequent exposure for 10 minutes to acidified (50 mM HCl) 80 mM sodium taurocholate (NaT). The protection afforded by sucralfate was abolished by inhibition of cyclooxygenase activity but restored by sucralfate. In this study we demonstrate that indomethacin pretreatment decreases both the depth (in microns) and magnitude (in pH units) of the juxtamucosal pH gradient, but that sucralfate restores these parameters to levels characteristic of normal mucosae. The cytoprotective effect of sucralfate is thus prostaglandin-independent and, at least in part, a consequence of sucralfate-induced increases in the thickness of the juxtamucosal pH gradient/unstirred layer. We have also examined the ability of sucralfate to prevent the otherwise inevitable development of hemorrhagic erosions when it was applied after the gastric mucosa was exposed to NaT. When 100 mg sucralfate in 50 mM HCl was applied for 10 minutes, without stirring, subsequent to a 10-minute exposure of the mucosa to NaT, the average lesion area was reduced from about 15% to less than 3%. Unlike its cytoprotective property, the ability of sucralfate to accelerate the recovery process after damage was abolished by indomethacin pretreatment. Studies using antimony microelectrodes revealed that indomethacin pretreatment resulted in reductions in both the depth and magnitude of the pH gradient that resulted from plasma efflux from the mucosa after exposure to the acidified bile salt. These studies demonstrate that sucralfate is capable not only of prevention or attenuation of acute damage when administered prior to damaging agents, but is also capable of arresting the sequence of events that produces hemorrhage in the previously inflamed or damaged stomach.

Animals↗
PubMed1975

Stress ulceration and the gastric mucosal barrier.

The role of the gastric mucosal barrier in the pathogenesis of post-traumatic stress ulcerations is far from clear. Clinical studies on critically ill patients have shown disrupted gastric mucosal barriers with hydrogen ion back diffusion, but no correlation has been made between these findings and gastric erosions. In addition, numerous assumptions concerning gastric secretions, pyloric loss and esophageal contributions to the assayed gastric juice have to be made in these patients. There is contradictory experimental evidence concerning the theory that gastric mucosal ischemia or hypotension disrupts the normal gastric mucosal barrier. In subhuman primate studies, there is no increased back diffusion acid during hypotension or during the reinfusion periods. Even though there may not be increased permeability to H+, the presence of acid is a requirement for the development of stress ulcerations. The role of agents such as bile salts and aspirin is clearer. If these agents are present, increased back diffusion of acid is likely, but its role in the pathophysiology of post-traumatic gastric erosion awaits further clarification.

Animals↗
PubMed1979

Significance of antral pH for gastrin release by insulin hypoglycemia in duodenal ulcer patients.

The significance of antral pH for the basal serum level of immunoreactive gastrin and for the release of gastrin during insulin hypoglycemia has been studied in duodenal ulcer (DU) patients. To permit paired comparisons, 14 DU patients underwent two or three tests with insulin. Venous blood samples were collected at fixed intervals for determination of gastrin (radioimmunoassay). In the first insulin test, the gastric juice was aspirated; in the second test, the stomach was perfused with citrate-phosphate buffer, pH 7.0; and in the third test the stomach was perfused with 0.1M HCl, pH 1.0. The rate of buffer or acid perfusion was adjusted, and the pH of the perfusate was kept above 5.0 and below 1.3, respectively. Gastric perfusion with buffer or acid for 1 hour did not affect the basal serum gastrin level, nor did perfusion with buffer for 3 hours. Insulin hypoglycemia stimulated acid secretion and produced a significant integrated serum gastrin response during gastric aspiration, but the gastrin response was four times greater during buffer perfusion. Acid perfusion abolished the gastrin response. From our previous and present findings, it is concluded that the gastrin in serum during basal conditions is of extra-antral origin and is independent of antral pH. Insulin hypoglycemia releases antral gastrin by a pH-sensitive mechanism in DU patients; the release is suppressed at pH 1.3 or less and also is markedly inhibited when the gastric juice is aspirated.

Adult↗
PubMed1993

Chronic pulmonary aspiration in children.

According to established diagnostic and therapeutic guidelines for chronic pulmonary aspiration, clinical suspicion is raised by coughing and choking with feeding, coughing during sleep, recurrent pneumonia, failure to thrive, and radiologic signs of chronic lung injury. The upper gastrointestinal series accurately defines anatomy and function, can differentiate between direct and reflux aspiration, and identifies conditions that predispose to aspiration. Gastroesophageal scintigraphy lacks anatomic detail but increases observation time, may differentiate between direct and reflux aspiration, and identifies delayed gastric emptying and gastroesophageal reflux. The lipid-laden macrophage index improves identification of aspiration, but cannot differentiate between direct and reflux aspiration. The esophageal pH probe identifies gastroesophageal reflux. Treatment options include medical therapy (thickened feedings, prone positioning, and metoclopramide) and surgical intervention (gastrostomy, fundoplication, and definitive correction of predisposing conditions). Therapy is determined by severity of illness and results of diagnostic evaluation.

Bethanechol↗
PubMedDate not supplied

Predicting serum gastrin levels among men during Ramadan fasting.

Increased gastric acidity is common when fasting during Ramadan. Our study aimed to develop a regression equation to predict fasting serum gastrin levels using parameters commonly analysed in clinical laboratories. Fasting blood samples from six men were taken on days 1, 10, 19, 26 and 28 of Ramadan. Serum gastrin, total cholesterol, urea and uric acid were analysed. All 5 samples from each man were included in multiple regression analysis and the prediction equation obtained was: serum gastrin, pg/mL = 198.27-0.199 total cholesterol (mg/dL) + 2.525 urea (mg/dL)--103.238 uric acid (mg/dL) + 10.923 uric acid (mg/dL)2 + 3.683 body mass index, r2 = 0.75, P < 0.001. This equation might be used to estimate gastrin levels and plan dietary and medicinal measures to avoid high gastric acidity during Ramadan.

Adult↗
PubMed1992

Somatostatin in gastric juice in normal subjects and patients with duodenal ulcer.

Somatostatin in gastric juice was determined in normal subjects and patients with duodenal ulcer. Gel exclusion chromatography of gastric juice revealed that the main immunoreactivity existed at the position of somatostatin-14. A large amount of somatostatin was present in gastric juice, and the quantity increased following tetragastrin stimulation. Furthermore, there was a good inverse correlation between somatostatin concentration and acidity of gastric juice; however, there was no difference between normal subjects and patients with duodenal ulcer in the amount of somatostatin released into gastric juice.

Adult↗
PubMed2001

Helicobacter pylori infection in the cat: evaluation of gastric colonization, inflammation and function.

BACKGROUND: Further elucidation of the consequences of Helicobacter pylori infection on gastric mucosal inflammation and gastric secretory function would be facilitated by an animal model that is susceptible to infection with H. pylori, is broadly similar in gastric physiology and pathology to people, and is amenable to repeated non-invasive evaluation. The goal of this study was to examine the interrelationship of bacterial colonization, mucosal inflammation and gastric secretory function in cats with naturally acquired H. pylori infection. MATERIALS AND METHODS: Twenty clinically healthy cats with naturally acquired H. pylori infection (cagA-, picB) and 19 Helicobacter-free cats were evaluated. Gastric colonization was determined by tissue urease activity, light microscopy, culture and PCR. The mucosal inflammatory response was evaluated by light microscopy, and by RT-PCR of the pro-inflammatory cytokines IL-1alpha, IL-1beta, IL-8 and TNF-alpha in gastric mucosa. Gastric secretory function was assessed by measuring pentagastrin-stimulated acid secretion, fasting plasma gastrin, and antral mucosal gastrin and somatostatin immunoreactivity. RESULTS: H. pylori colonized the pylorus, fundus and cardia in similar density. Bacteria were observed free in the lumen of gastric glands and were also tightly adherent to epithelial cells where they were associated with microvillus effacement. Mononuclear inflammation, lymphoid follicle hyperplasia, atrophy and fibrosis were observed primarily in H. pylori-infected cats, with the pylorus most severely affected. Neutrophilic and eosinophilic infiltrates, epithelial dysplasia, and up-regulation of mucosal IL-1beta and IL-8 were observed solely in infected cats. Fasting plasma gastrin concentrations and pentagastrin-stimulated acid output were similar in both infected and uninfected cats. There was no relationship of bacterial colonization density or gastric inflammation to plasma gastrin concentrations or gastric acid output. CONCLUSIONS: The pattern of colonization and the mucosal inflammatory response in cats with naturally acquired H. pylori are broadly similar to those in infected people, particularly children, and non-human primates. The upregulation of IL-8 in infected cats was independent of cagA and picB. Our findings argue against a direct acid-suppressing effect of H. pylori on the gastric secretory-axis in chronically infected cats.

Animals↗
PubMed1997

Efficacy of omeprazole one year after cure of Helicobacter pylori infection in duodenal ulcer patients.

OBJECTIVE: We have previously shown that, in duodenal ulcer patients, pH control by omeprazole is less pronounced after cure of Helicobacter pylori infection. The present study was designed to test the hypothesis that this response to omeprazole persists 1 yr after cure of H. pylori infection. METHODS: In 12 duodenal ulcer patients, intragastric acidity was measured with a glass electrode during treatment with omeprazole (20 mg) once daily before, and 4-6 wk and 1 yr after, cure of H. pylori infection. H. pylori infection was assessed by [13C]urea breath test, culture, histology (Warthin Starry stain), and rapid urease test. RESULTS: Cure of H. pylori infection resulted in a lowered pH during omeprazole treatment. This effect persisted after 1 yr. Median 24-h gastric pH before H. pylori treatment was 5.6; 4-6 wk after cure of the infection it was 2.9 (p = 0.003), and 1 yr after cure of the infection it remained unchanged (pH = 2.5; p = 0.5). Accordingly, twice as much time was spent above pH 3 and pH 4 before H. pylori treatment than 1 or 12 months after cure (percent of time > or = pH 3: 82.7 vs. 49.7 vs. 43.1; percent of time > or = pH 4: 72.7 vs. 38.3 vs. 26.4). CONCLUSION: In duodenal ulcer patients, cure of H. pylori infection resulted in a marked rapid and persistent decrease of the pH increasing effect of omeprazole. Therefore, H. pylori is a determinant of the pH achieved in response to omeprazole treatment in duodenal ulcer patients.

Adult↗
PubMed1993

[Value of antral mucosectomy, selective proximal vagotomy and a combination of the 2 procedures in serum gastrin production and inhibition of stomach acid. An experimental study].

This experimental study was aimed at determining the volume and acidity produced by the normal stomach, following antral mucosectomy (MA), proximal selective vagotomy (VSP) and combination of both procedures. In 10 mongrel dogs, a double-lumen tube was placed in the stomach under general anesthesia. One of the lumen was rinsed with a constant flow and the other retrieved the gastric secretion. Gastric secretion and acidity were calculated every 10 minutes for 120 minutes. At 60 minutes, pentagastrin was injected. After these controls, a MA was carried out in half the animals and a VSP in the other half. 6 and 12 weeks postoperatively, the same controls were repeated. The dogs were then submitted to the operation of the other group. Following MA and pentagastrin stimulation, the gastric secretion (volume) is not modified with regard to the preoperative levels. On the other hand, after VSP, pentagastrin stimulation induces only a small volume response. The vagus thus seems to be involved in liquid secretion of the stomach. Following MA, pentagastrin stimulation lowers gastric pH at 6 weeks but not at 12 weeks postoperatively. Gastrin is known to have a trophic effect on the oxyntic mucosa. This effect disappears in a few weeks and explains these different figures. Following VSP, gastric acidity decreases and plasmatic gastrin increases. In this situation, pentagastrin directly acts on a trophic mucosa and produces the important lowering of the gastric pH. Finally, after MA, pentagastrin induces an increase in plasmatic gastrin. This effect seems to be mediated by central stimulation of the nuclei of the vagus nerve.

Animals↗
PubMed1976

[Practical value of gastric intubation during peptic ulcer. Analysis of 410 cases, after Histalog stimulation].

This study was carried out in 410 subjects, collecting gastric fluid for one hour, after 15 minutes emptying and one hour, after 15 minutes emptying and one hour's study of basal secretion using, as stimulant, Histalog at a maximal dose of 2 mg/kg without exceeding 130 mg. The object of this statistical analysis was to determine the average figures and the standard deviations of the volumes of secretions, together with those of the output of hydrogen ions in 5 groups of subjects: controls (60), gastric ulcers (38), duodenal ulcers (200), patients suspected of duodenal ulcer (60) or affected by dyspeptic syndrome without radiological nor endoscopic lesions (52). In the normal subject, the hydrochloric acid output was situated between 5 and 27 mEq. The diagnosis of duodenal ulcer was very unlikely when secretion was less than 9 mEq in man and almost certain above 30 mEq.

Adult↗
PubMed1978

Vagal innervation of the bypassed stomach following gastric bypass.

Gastric bypass, a 90% gastric exclusion, has been used successfully for surgical treatment of morbid obesity since 1967. Early concern as to its ulcerogenic potential has not materialized, but the physiological activity of the excluded stomach has not been studied fully. To determine whether the excluded segment retained any vagal innervation, 25 patients underwent preoperative Hollander tests of their intact stomachs. The test was repeated after operation, after the patients had resumed normal oral intake. Postoperative specimens were collected from a gastrostomy placed in the excluded stomach at the time of the gastric bypass. Percentage changes in volume and total acid for both the intact and excluded stomachs followed the same pattern with insulin injection after 45 minutes at both testings, pH values were identical. These observations, which indicate vagal innervation of the excluded stomach, together with previously published histalog acid-response data and the observed marginal ulcer incidence of one per 193 years of patient follow-up, demonstrate that normal gastric physiology is maintained after bypass and confirm that it is not an ulcerogenic procedure.

Gastric Acidity Determination↗
PubMed1996

Stimulation of acid secretion in rat stomach following exposure to taurocholate in the presence of the nitric oxide synthase inhibitor.

1. The role of nitric oxide (NO) in the acid secretory response of the rat stomach following damage was investigated. A rat stomach was mounted in an ex-vivo chamber, perfused with saline, and the potential difference (PD), luminal pH, acid and HCO3- responses were measured before and after the mucosal exposure to 20 mM taurocholate (TC) for 30 min, with or without pretreatment with NG-nitro-L-arginine methyl ester (L-NAME). 2. Exposure of the stomach to TC caused a reduction of PD, a decrease of acid secretion and an increase in luminal HCO-. Pretreatment with L-NAME did not affect such PD and HCO3- responses, but completely attenuated the decreased acid secretory response and rather enhanced this secretion. 3. These effects of L-NAME were significantly antagonized by the co-administration of L-arginine but not D-arginine. The enhanced acid secretory response in the presence of L-NAME was significantly inhibited by prior administration of cimetidine or FPL-52694 (a mast-cell stabilizer). 4. The mucosal exposure to TC significantly decreased the number of mucosal mast cells and increased the luminal histamine output. 5. Damage in the stomach may activate the histamine-dependent acid stimulatory pathway in addition to the NO-dependent inhibitory mechanism, although the latter effect overcomes the former, resulting in a decrease of acid secretion. L-NAME unmasks the stimulation of acid secretion by suppressing the inhibitory pathway.

Animals↗
PubMedDate not supplied

Effects of intravenously administrated omeprazole on gastric juice pH and gastric ulcer scores in adult horses.

The study was performed to evaluate the efficacy of omeprazole powder in sterile water, administered intravenously, on gastric juice pH in adult horses with naturally occurring gastric ulcers. Omeprazole (0.5 mg/kg, IV) was administered once daily for 5 days to 6 adult horses with gastric ulcers. Gastric juice was aspirated through the biopsy channel of an endoscope and pH was measured before and 1 hour after administration of omeprazole on day 1, and then before and after administration of omeprazole on day 5. Gastric ulcer scores were recorded on day 1 before administration of omeprazole and on day 5, 23 hours after the 4th daily dose. Gastric juice pH and ulcer scores were compared between the times. When compared with the pre-injection value (2.01 +/- 0.42), mean +/- SD gastric juice pH was significantly higher when measured 1 hour after administration of the initial dose (4.35 +/- 2.31), and before (5.27 +/- 1.74) and 1 hour after (7.00 +/- 0.25) administration of omeprazole on day 5. Nonglandular gastric ulcer number score significantly decreased from a mean +/- SD of 3.2 +/- 0.80 to 2.0 +/- 1.1, but nonglandular gastric ulcer severity score remained the same. Few glandular ulcers were seen in the study, and scores did not change. Because of its potent and long duration of action on gastric juice pH, this intravenous formulation of omeprazole may show promise for treatment of equine gastric ulcer syndrome (EGUS) in horses with dysphagia, gastric reflux, or other conditions that restrict oral intake of omeprazole paste. Aspiration of gastric juice and measurement of pH can be of use to determine whether the desired pH > 4.0 has been reached after omeprazole treatment.

Animals↗