Changes In Gastric Secretion Research Articles

Autoimmune gastritis studies and gastric cancer: True renaissance or bibliometric illusion.

A bibliometric analysis of studies dedicated to autoimmune gastritis (AIG) recently published demonstrated a noteworthy surge in publications over the last three years. This can be explained by numerous publications from different regions of the world reporting the results of several studies that stimulated reassessment of our view of AIG as a precancerous condition. Follow-up studies and retrospective analyses showed that the risk of gastric cancer (GC) in AIG patients is much lower than expected if the patients ever being infected with Helicobacter pylori (H. pylori) were excluded. The low prevalence of precancerous lesions, such as the incomplete type of intestinal metaplasia, may explain the low risk of GC in AIG patients because the spasmolytic polypeptide-expressing metaplasia commonly observed in AIG does not involve clonal reprogramming of the gastric gland and can be considered as an adaptive change rather than a true precancerous lesion. However, changes in gastric secretion due to the progression of gastric atrophy during the course of AIG cause changes in the gastric mic-robiome, stimulating the growth of bacterial species such as streptococci, which may promote the development of precancerous lesions and GC. Thus, Streptococcus anginosus exhibited a robust proinflammatory response and induced the gastritis-atrophy-metaplasia-dysplasia sequence in mice, reproducing the well-established process for carcinogenesis associated with H. pylori. Prospective studies in H. pylori-naïve patients evaluating gastric microbiome changes during the long-term course of AIG might provide an explanation for the enigmatic increase in GC incidence in the last decades in younger cohorts, which has been reported in economically developed countries.

Observations of changes in gastric secretion under the influence of kumis therapy

Observations of changes in gastric secretion under the influence of kumis therapy

Changes of Gastric Secretion after Bolus and Slow Intravenous Administration of Bombesin and Neurotensin

Objectives:The aim of the present study was to evaluate the changes caused by intravenous administration of regulatory peptides, bombesin (BBS) and neurotensin (NT), on gastric secretion, serum gastrin, and plasma levels of bombesin-1ike immunoreactivity (BLI) and neurotensin. Materials and methods: Fourteen dogs underwent an upper gastrointestinal tract operation and a Pavlov pouch for the concentration of gastric fluids was formed. The experimental animals were divided into two groups. Peptides were given one month after the second operation and after fasting for 12 hours. In group A, the effects of BBS were studied after a rapid 1 ìg/kg body weight dose and a slow 30´ 0.5 ìg/kg body weight dose administration intravenously. Correspondingly to group B the effects of NT were studied in the same way. Results:The rapid intravenous infusion of BBS caused a very significant increase in gastrin levels, BLI in plasma, volume and HCl of the gastric fluids. The same results, plus a significant decrease in gastric pH, were observed following slow intravenous infusion of BBS. Concerning the NT, rapid administration caused a significant decrease in the volume of gastric fluids. Slow NT administration of caused a significant reduction in gastric fluid volume and in HCl. On the contrary, pH was significantly increased. Conclusion:Bombesin increases plasma gastrin levels and HCl secretion. Neurotensin administration causes a decrease in HCl secretion without affecting gastrin levels in plasma.

Age-Dependent Association among Helicobacter pylori Infection, Serum Pepsinogen Levels and Immune Response of Children to Live Oral Cholera Vaccine CVD 103-HgR

BackgroundThrough its effects on gastric secretion, we hypothesized that Helicobacter pylori infection may influence oral immunization. Accordingly, we examined the association between H. pylori infection, serum pepsinogen (PG) (measures for H. pylori gastritis) and vibriocidal antibody (a correlate of protection) seroconversion following oral immunization with CVD 103-HgR live cholera vaccine among children of different ages.MethodsSera from 422 Chilean children who were vaccinated with a single dose of CVD 103-HgR were tested by ELISA for serum IgG antibodies to H. pylori, PG I and PG II levels and antibodies to Shigella flexneri 2a lipopolysaccharide and hepatitis A virus (as markers of low socioeconomic status and exposure to enteric pathogens).ResultsThe likelihood of vibriocidal antibody seroconversion following vaccination with CVD 103-HgR was significantly decreased in H. pylori-seropositive children age 6 months to 4 years with PG II>8 µg/L (adjusted OR 0.14 (95% CI 0.03–0.61; P = 0.009), and also in H. pylori seropositives with lower PG II level (adjusted OR 0.34, 95% CI 0.14–0.83; P = 0.017), compared to H. pylori-seronegatives. H. pylori-seropositive children aged 5–9 years with serum PG I>30 µg/L (indicating more severe gastritis) had higher odds of vibriocidal seroconversion than those with lower PG I levels (adjusted OR 4.41, 95%CI 1.26–15.38; P = 0.02). There was no significant association between exposures to S. flexneri 2a or hepatitis A virus and vibriocidal seroconversion.ConclusionsAs H. pylori gastritis progresses with increasing pediatric age in developing country venues, changes in gastric secretion ensue that we believe explain the observed differences in age-related immune responses to immunization with live oral cholera vaccine. The effect of H. pylori and changes of gastric acid secretion on the immunogenicity of various oral vaccines should be studied in different developing, transitional and industrialized country settings.

Variation of Drug Kinetics in Pregnancy

Significant changes in the physiological and biotransformation processes that govern pharmacokinetics occur during pregnancy. Consequently, the disposition of many medications is altered in gestation and the efficacy and toxicity of drugs used by pregnant women can be difficult to predict or can lead to serious side effects. Gastrointestinal absorption and bioavailability of drugs vary due to changes in gastric secretion and small intestine motility. Various pregnancy-related hemodynamic changes such as an increase in cardiac output, blood volume, the volume of distribution (Vd), renal perfusion and glomerular filtration may affect drug disposition and elimination, and can cause increase or decrease in the terminal elimination half-life of drugs. Changes in maternal drug biotransformation activity also contribute to alterations in pharmacokinetics of drugs taken in pregnancy. Therefore, pregnant women may require different dosing regimens or their adjustment than both men and non-pregnant women. In addition, the prenatal pharmacotherapy is unique due to the presence of feto-placental unit. Considerations regarding transplacental pharmacokinetics and safety for the developing fetus are thus essential aspects of medication in pregnancy. The aim of this review is to summarize major physiological and biotransformation changes associated with pregnancy that affect pharmacokinetics in pregnant women. In addition, we point out the most important examples of altered kinetics of drugs administered in pregnancy with mechanistic explanation of the phenomena based on maternal adaptation in pregnancy.

Nigella sativa seeds: Folklore treatment in modern day medicine

<i>Nigella sativa</i> seeds: Folklore treatment in modern day medicine

Effect of zinc sulphate on indomethacin Induced changes in gastric secretion and Ulceration in male albino rats

Effect of zinc sulphate on indomethacin Induced changes in gastric secretion and Ulceration in male albino rats

Abomasal secretion in sheep receiving adult Ostertagia circumcincta that are prevented from contact with the mucosa

Aims. Both adult and larval Ostertagia circumcincta infections raise abomasal pH and serum gastrin and pepsinogen concentrations, either because of physical effects of the worms or from their chemical secretions. The study was designed to examine whether adult worms require contact with the gastric mucosa to effect changes in gastric secretion. Methods. Abomasal pH and serum gastrin and pepsinogen concentrations were measured in four groups of sheep: Group A (n = 4): abomasal contents containing about 18 000 adult O. circumcincta were obtained from donor sheep, concentrated and infused into 5 µm mesh porous bags attached to surgically implanted abomasal cannulae. A second worm transplantation was carried out 1 week later to assess worm survival after 16 hours. Group B (n = 4): about 9000 adult worms, recovered after migration out of abomasal contents set in agar, were placed in small 5 µm mesh bags which were inserted through indwelling abomasal cannulae and left for 3 days. Group C (n = 2): about 9000 adult worms from the population recovered from agar were infused through abomasal cannulae which allowed. free movement in the abomasum. Group D (n = 3) was left uninfected. Results. Worms transplanted directly into the abomasum (Group C) caused rapid and marked effects on abomasal secretion. Adult O. circumcincta died within 16 hours of transfer into the abomasum when they were restrained within porous bags. Nevertheless, in sheep receiving 18 000 worms, abomasal pH increased soon after new feed was presented on Days 1, 2 and 4 after worm transfer; serum gastrin was elevated in three sheep from 113 hours and serum pepsinogen increased in one animal. Sheep receiving 9000 worms showed similar trends but the results were equivocal. Conclusions. Adult O. circumcincta prevented from physical contact with the gastric mucosa by restraint in porous bags are able to raise abomasal pH. This study implicates parasite excretory-secretory products in mediating changes in gastric secretion caused by adult abomasal worms.

Increased gastric acid secretion after massive small bowel resection is related to a decrease in enterogastrones.

The reported increase of gastric secretion after small bowel (SB) resection is controversial. To determine the effect of SB resection on gastric acid secretion we studied basal and dose step pentagastrin-stimulated gastric acid secretion as well as basal serum gastrin, secretin, neurotensin and postprandial gastrin levels in 12 dogs, before and after resection of 60% of the intestine representing both proximal (n = 6) and distal (n = 6) SB. Rat bioassay was also performed to rule out the presence of unknown gastric secretagogues in the blood. Proximal SB resection produced a significant increase in basal and low dose (100 ng/kg/h) pentagastrin-stimulated gastric acid secretion (ED50 = 1,110 vs. 720 ng/kg/h after resection). However, no significant changes in gastric secretion were observed after distal SB resections. Neither proximal nor distal SB resection altered basal or postprandial serum gastrin levels. Proximal SB resection reduced serum secretin levels (229 +/- 38 vs. 134 +/- 16 pg/ml, p < 0.05) but did not alter neurotensin levels. Rat bioassay failed to reveal a circulating secretagogue after SB resections. We conclude that proximal but not distal SB resection increases basal and submaximally stimulated gastric acid secretion. Such an effect may be due to the observed decrease in circulating secretin levels.

Intracerebroventricular infusion of neurotensin suppresses gastric acid secretion in dogs.

Synthetic neurotensin (NT) was infused intracerebroventricularly in 14 mongrel dogs to study the effects of the peptide on gastric secretion and on gastrin and NT levels. The infusion was performed with a specific apparatus, and gastric fluid was collected with a Pavlov pouch. NT was given in two series of experiments: as a bolus intracerebroventricular injection of 269.8 pmol/kg and as a continuous intracerebroventricular infusion at a rate of 539.6 pmol/kg/h for 30 min. The bolus injection caused a very significant decrease of gastric fluid volume, a significant decrease of HCl output and a significant increase of its pH, while serum immunoreactive gastrin increased significantly. The continuous infusion of NT caused similar changes in gastric secretion. The plasma NT levels did not change. In conclusion, the intracerebroventricular administration of NT increases the serum gastrin levels, decreases the volume and HCl content of gastric fluid, and increases its pH.

Changes in Gastrointestinal, Pancreatic, Biliary, and Hepatic Function with Aging

The understanding of "normal" aging of the gastrointestinal tract, pancreas, and hepatobiliary system is confounded by the difficulty in identifying healthy elderly subjects for study. There appear to be predictable changes in gastric secretion and emptying, intestinal and pancreatic morphology, colorectal motility, and hepatic mass and blood flow with aging. However, the functional significance of these changes is variable. Further investigations will be necessary to resolve currently conflicting data, and validation of animal models of aging will enhance future research into these areas.

Changes in Gastric Secretion after Intracerebroventricular Infusion of Bombesin in Dogs

Synthetic bombesin (BBS) was infused intracerebroventricularly in 14 mongrel dogs, to study the effects of the peptide on gastric secretion and on gastrin and neurotensin levels. The infusion was performed with a specific apparatus, and gastric fluid was collected with a Pavlov pouch. BBS was given in two series of experiments: as a bolus intracerebroventricular injection of 308.6 pmol/kg and as a continuous intracerebroventricular infusion at a rate of 617.3 pmol/kg/h for 30 min. The bolus injection caused a very significant decrease of gastric fluid volume, a significant decrease of HCl output, and a significant increase of its pH, while serum immunoreactive gastrin increased significantly. The continuous infusion of BBS caused similar changes in gastric secretion. The plasma neurotensin levels did not change. In conclusion, the intracerebroventricular administration of BBS increases the serum gastrin levels, decreases the volume and HCl content of gastric fluid, and increases its pH.

Causes and consequences of hypochlorhydria in the elderly.

A workshop entitled "Causes and Consequences of Hypochlorhydria in the Elderly," cosponsored by the National Institute on Aging; the National Institute of Diabetes, Digestive and Kidney Diseases; and the USDA Human Nutrition Research Center on Aging, was held on September 28 and 29, 1987, in Bethesda, Maryland. The workshop was organized following discussions by Drs. Holt, Rosenberg, and Russell, members of the Council on Aging of the American Gastroenterological Association, and Drs. Evan Hadley and Van Hubbard of the NIH. The conference was introduced as an opportunity to review the state of knowledge about hypoand achlorhydria and the research opportunities in respect to nutritional and metabolic consequences. Dr. John Fordtran (Baylor University Medical School) began by reviewing age-related changes in gastric secretion. He noted there was no uniform definition of hypochlorhydria in the literature. He suggested that a reasonable definition of hypochlorhydria was: acid production following a standard meal stimulus in well-defined normal subjects which was two standard deviations below the mean. The normals would need to be a group of subjects with normal gastric biopsies and no evidence of active Campylobacter infection. In early life, gastric acid output reaches adult levels by 24 weeks of age. The average rate of acid secretion by the stomach does appear to fall with advancing age but this may well be due to a higher prevalance of hypochlorhydria in individual subjects among this age group. Indeed,

Inhibition of gastric secretion in guinea pig by relatively low dose ionizing radiation.

We evaluated the effect of a single dose of ionizing radiation on gastric secretion in awake guinea pigs equipped with a permanent gastric cannula. Changes in gastric secretion were measured using a dye dilution technique. Infusion of histamine increased acid and fluid output and there was a positive correlation (r = 0.93) between the two. Total body irradiation with 400 cGy, like cimetidine, suppressed acid and fluid secretion under basal conditions and during histamine stimulation by 50-90%. Recovery from the radiation damage was only partial after one week. Irradiation inhibited the rise in gastric juice volume during histamine stimulation and also reduced the normal gain in body weight of the guinea pig. These results demonstrate that ionizing radiations have an immediate and long lasting effects on the gastric mucosal function of the guinea pig.

The pharmacokinetics of antiarrhythmic agents in pregnancy and lactation.

The pharmacokinetics of various drugs may be profoundly altered during different stages of pregnancy, parturition, and lactation. Gastrointestinal absorption or bioavailability of drugs may vary due to changes in gastric secretion and motility. Various haemodynamic changes such as an increase in cardiac output, blood volume, and renal plasma flow may affect drug disposition and elimination. The increase in blood volume and total body water which occurs during pregnancy can alter the volume of distribution for various drugs. Although exact quantifications are not easy, these changes in pharmacokinetic parameters should be considered when dosing antiarrhythmic agents in pregnant women. Plasma protein concentrations and drug binding capacity are altered in the mother and fetus as pregnancy advances. With highly protein bound drugs, these changes may be clinically significant, as the pharmacological efficacy and toxicity are presumed to be related to the concentration of free drug in both the mother and fetus. In some instances, the fetus may be susceptible to greater drug toxicity as free drug concentrations may be underestimated by measurement of total drug concentrations. Changes in maternal drug metabolism and metabolism by the fetoplacental unit also contribute to alterations in the pharmacokinetics of drugs. As the placenta contains many metabolising enzymes, biotransformation of drugs at this site could potentially convert a drug into an active metabolite, or prevent fetal exposure to a toxic drug. Placental transfer of drugs, leading to toxicity in the fetus, is a major concern in the pharmacological management of the pregnant patient. The passage of individual drugs will vary depending on their apparent volumes of distribution, degree of protein binding the rates of metabolic conversion and excretion within the placenta and fetus, the pH difference between the maternal and fetal fluids, and maternal haemodynamic changes. Drug properties such as lipid solubility, protein binding characteristics, and ionisation constant (pKa) also influence the placental passage of drugs. For weakly basic antiarrhythmic agents, the fetal drug concentration may potentially exceed the maternal plasma concentration when the fetal pH is lowered as in the case of fetal acidosis; this is due to 'ion trapping'. Additionally, higher free drug concentrations of these basic drugs may exist, due to decreased alpha 1-acid glycoprotein concentration and binding affinity in the fetus. Lignocaine (lidocaine) has been shown to enter fetal plasma rapidly with fetal-maternal concentration ratios in the range of 0.52 to 0.66.(ABSTRACT TRUNCATED AT 400 WORDS)

The sites and mechanisms of action of 2-DI- n-propylamino-5,6-dihydroxytetralin in the hypothalamus of the rat to modify gastric secretion

Rats were implanted with chronically indwelling gastric and intracerebral cannulae for the analysis of the hypothalamic sites and mechanisms of action of the dopamine agonist, 2-di- n-propylamino-5,6-dihydroxytetralin, to reduce the volume of gastric secretion and concentration of add. The hypothalamic areas most sensitive to the actions of the tetralin compound to modify gastric secretion were the ventromedial and dorsomedial nuclei. Movement of the injection site 0.5 or 1.0mm away from the ventromedial and dorsomedial nuclei in the anterior, posterior or lateral direction led to reduced effectiveness, or loss of action. In a study restricted to the ventromedial nucleus of the hypothalamus, the tetralin compound (0.1–5μg) was shown to cause dose-dependent changes in gastric secretion, the reduction in concentration of acid being antagonised by the neuroleptic agents, sulpiride, metoclopramide, cis-flupenthixol and haloperidol, and by the α 2-adrenoceptor antagonist, yohimbine injected at the same site. The reduction in secretory volume was antagonised by propranolol. Thus, a locus specificity was shown for the action of the tetralin compound in the dorsomedial and ventromedial hypothalamic nuclei of the rat, to reduce the volume of gastric secretion and concentration of acid. Such actions, as assessed in the ventromedial nucleus, are initiated via neuroleptic-sensitive, dopamine receptor mechanisms with additional involvement of α 2-adrenoceptors in the control of change in concentration of acid, and β-adrenoceptors in the change in volume of secretion.

Pancreatic surgery, gastric secretion and ulcers in the rat. Increased ulcer development following pancreatic half resection or duct occlusion.

In the rat, both partial resection of the pancreas and occlusion of the side branches of the biliodigestive duct were investigated with respect to their influence on gastric secretion (acid, pepsin, sodium), gastric mucosal blood flow (MBF), development of gastric ulcers, and gastrin and somatostatin in the blood. On the 14th postoperative day the exocrine pancreatic function is reduced and ulcer index and severity are significantly enhanced. There are no simultaneous changes in gastric secretion or MBF. Aortal gastrin was decreased and somatostatin was unchanged. We conclude that: in the rat, reduction of exocrine pancreatic function should be considered an ulcerogenic factor; factors others than gastric hypersecretion or reduced MBF are responsible for ulcer formation, and an etiological role of either circulating gastrin or somatostatin is doubtful.

Gastric secretion and mucosal lesions in morphine-dependent rats.

The gastric mucosa and basal gastric secretion of morphine-dependent rats with pyloric occlusion were examined. Morphine tolerance and dependence were induced by administering increasing concentrations of morphine sulphate in the drinking water for 3 weeks, and were confirmed by a decreased analgesic response to morphine in the tail-immersion test and by occurrence of a naloxone-precipitated withdrawal syndrome, respectively. It was found that although the basal gastric secretion of morphine-dependent rats was not significantly different from that of naive animals, the former group showed a significantly higher gastric glandular mucosal ulcer index. Intraperitoneal injection of naloxone induced significant withdrawal effects but did not produce significant changes in gastric secretion or in ulcer index.

Gastric secretory conditions and plasma gastrin levels in rats after prolonged treatment with cimetidine.

Effects of 4 weeks of treatment with oral cimetidine, 100 mg/kg twice daily, on gastric secretion and plasma gastrin levels were studied in rats. Pylorus ligation-induced and pentagastrin-stimulated gastric secretions were little changed at days 1, 3, and 10 after cessation of cimetidine treatment as compared to the controls. Histamine-stimulated acid secretion was significantly higher in the cimetidine-treated group than in the controls at day 3 after cimetidine treatment but was unchanged at days 1 and 10. A single oral administration of cimetidine at 100 mg/kg significantly increased plasma gastrin levels 4 hr after the treatment in refed rats but not at 2 and 8 hr later. Plasma gastrin levels significantly decreased at days 3 and 10 after cessation of cimetidine treatment as compared to the controls. Thus, while prolonged treatment with cimetidine induces a transient increase in response of parietal cells to histamine and a reduction of food-stimulated gastrin release, it does not seem to induce other appreciable changes in gastric secretion.

Changes in gastric secretion with time after vagotomy and the relationship to recurrent duodenal ulcer.

We studied 29 patients who had gastric secretion tests after a vagotomy for duodenal ulcer. There were 14 patients who developed a recurrent duodenal ulcer during the follow-up period and 15 patients who remained free from recurrence. Insulin-stimulated gastric secretion increased with time in the recurrent ulcer group, but not in the group with a satisfactory outcome. On the basis of our results, post-vagotomy patients could be divided into three groups. The first group had a high secretion immediately after the operation and it remained high. The risk of recurrent ulcer in that group was about 50%. The second group had an initially low secretion which increased with time, and the risk of recurrent ulcer in that group was the same as for the first group. The third group had an early low secretion which did not increase with time and the risk of recurrence in this group was less than 5%.