Decrease In Gastric Acid Secretion Research Articles

Effect of Date (Phoenix Dactylifera L.) on Stimulated Gastric Acid Secretion in Wistar rats

Background: Peptic ulcer disease (PUD), encompassing gastric and duodenal ulcers is the most prevalent gastrointestinal disorder. The pathophysiology of PUD involves an imbalance between offensive factors like acid, pepsin and defensive factors such as nitric oxide and growth factors. The clinical evaluation of antiulcer drugs showed tolerance, incidence of relapses and side effects that make their efficacy arguable. Local folklore claims showed that Date (Phoenix Dactylifera L.) has a gastric beneficial role in humans. This study was therefore carried out to examine the effects of Dates on stimulated gastric acid secretion (GAS) in the Wister rats. Materials/Methods: Three groups of rats consisting of 5 rats (180- 200g) each were treated with aqueous undialyzed extract of Dates (1.5mg/kg, 2.5mg/kg and 4.0mg/kg) orally for 21 days, while the fourth group were given distilled water for the same number of days. At the last day of the treatment, the rats were fasted for 24 hours, anaesthetized with ketamine. GAS (mEq/l) induced by histamine, carbachol and pentagastrin administration was assessed by continuous perfusion technique. Data were analyzed using student's T-test and ANOVA at p≤ 0.05. Results: The aqueous extract of undialyzed Dates significantly decreased (p≤ 0.05) GAS induced by the histamine, carbachol and pentagastrin in a dose-dependent manner over 80 minutes period in all the treated groups. Conclusion: Date extract exhibited a graded dose-dependent decrease in gastric acid secretion. Keywords: Date, Gastric, Pentagastrin, Histamine and Carbachol

Na+-K+-2Cl- cotransporter 2 located in the human and murine gastric mucosa is involved in secretagogue-induced gastric acid secretion and is downregulated in lipopolysaccharide-treated mice

Na+-K+-2Cl- cotransporter (NKCC) is expressed at exceptionally high levels in gastric parietal cells. Bumetanide, a potent loop diuretic that blocks NKCC, usually causes a decrease in gastric acid secretion. Endotoxaemia causes hypochlorhydria in vivo, in which lipopolysaccharide (LPS) plays an important role. This study aimed to investigate the effect of NKCC2 on gastric acid secretion and its alteration in LPS-treated mice. The scanning ion-selective electrode technique and real-time pH titration combined with RNA interference were used to determine the effects of bumetanide on gastric acid secretion. Immunochemistry and Western blotting were performed to investigate the changes in NKCC2 expression in LPS-treated mice. Immunoreactivity of NKCC1 and NKCC2 was mainly observed near the basolateral and apical membranes of parietal cells, respectively. Pretreatment with bumetanide reduced the histamine-stimulated H+ flux in the mouse gastric mucosa. The apical, but not the basolateral, addition of bumetanide inhibited forskolin- or histamine/3-isobutyl-1-methylxanthine(IBMX)-induced gastric acid secretion. In vivo treatment with NKCC2 siRNA inhibited forskolin-induced acid secretion. Upon histamine stimulation, the majority of NKCC2 was targeted to the apical membrane in the gastric mucosa and in primary cultured parietal cells. The expression of NKCC2 and vesicle-associated membrane protein-2 (VAMP2), but not that of H+/K+-ATPase, was decreased in the gastric mucosa of LPS-treated mice. Blocking apical NKCC2, but not basolateral NKCC1, by bumetanide inhibited secretagogue-induced gastric acid secretion, during which the membrane trafficking of NKCC2 may be necessary. The downregulation of NKCC2 and VAMP2 may be related to the reduced gastric acid secretion induced by LPS.

EVALUATION OF GASTROPROTECTIVE EFFECT OF COENZYME Q 10 AND L - GLUTAMINE IN STRESS AND ETHANOL-INDUCED PEPTIC ULCER IN WISTAR RATS: A NOVEL PRECLINICAL STUDY

Objective: Coenzyme Q 10 (CoQ10) and L-glutamine have antioxidant property their role in peptic ulcer diseases is not well known. Hence, the aim of present study is to evaluate the gastroprotective role of CoQ10 and L-glutamine in stress and ethanol-induced peptic ulcers in Wistar albino rats.Methods: A total of 90 rats were used for the conduct of study in two experimental models, the stress- and the ethanol-induced ulcer model. Each model consists of eight groups with six rats in each group. Sucralfate and pantoprazole were used as standard drugs along with CoQ10 and L- glutamine as test drugs. Drugs were administered for 10 days in stress model and 7 days in case of ethanol model. Statistically analyzed using analysis of variance and post-hoc test with significance as p>0.05Results: CoQ10 and L- glutamine when used alone as well in combination with pantoprazole and sucralfate showed no ulcer formation. Test drugs showed decrease in gastric acid secretion, decreased total and free acidity levels, higher gastric pH, increased mucous secreting ability, higher levels of reduced glutathione levels in both tissue as well as blood and lower malondialdehyde levels when compared with pantoprazole and sucralfate suggestive of their antioxidative benefit, in both the models.Conclusion: Well-designed clinical trials can be done to evaluate the use of CoQ10 and L- glutamine in the treatment of peptic ulcer disease due to various etiology.

Seeds of Buchholzia coriacea in Diet Mitigate Ischemic Reperfusion–Induced Gastric Ulceration in Experimental Rats

ABSTRACTBuchholzia coriacea (B. coriacea) seeds, in folk medicine, have been documented to prevent gastric ulceration though the mechanism is not fully elucidated. To clarify this, the gastro-healing activities were investigated using graded incorporation of B. coriacea seeds in the diet. Male Wistar rats (150–200 g) were divided into 7 groups (n = 15): unulcerated untreated control, ulcerated untreated control, unulcerated B. coriacea low (10%), ulcerated B. coriacea low (10%), nulcerated B. coriacea high (25%), ulcerated B. coriacea high (25%), and ulcerated omeprazole-treated groups. Rats were fed with B. coriacea diets for 7 weeks; thereafter, ulcer was induced by ischemic reperfusion method. Daily body weight, gastric acid secretion, hematological parameters, stomach ulcer score, and biochemical and histological analyses were evaluated on days 0, 3, and 7 post–ulcer induction. Results were subjected to one-way analysis of variance (ANOVA) and presented as mean ± standard error of the mean (SEM); p ≤.05 was considered significant. Significant decreases were observed in mean body weight of B. coriacea–fed compared with control and omeprazole-treated groups from week 7. Ulcerated B. coriacea–fed showed significant decrease in gastric acid secretion by days 3 and 7 compared with ulcerated control groups. Malondialdehyde content was significantly decreased in ulcerated B. coriacea–fed compared with control and omeprazole–treated groups. Significant increases in hematological variables (notably platelet count), superoxide dismutase, catalase, and nitric oxide levels of B. coriacea–fed compared with control and omeprazole-treated groups by days 0 and 3 were observed. Histological evaluations further confirmed these observations. B. coriacea diet enhanced gastric healing activities on ischemic reperfused gastric ulcer. Increased platelet count and nitric oxide levels may play significant roles in this process.

Evaluation of Long Term Alcohol Consumption on Gastric Acid Secretion and the Histomorphometry of the Stomach in Adult Male Wistar Rats

This study was aimed at investigating to check the effects of long term consumption of varying concentrations of alcohol on gastric acid secretions and the histomorphometry of the stomach of adult male Wistar rats, and the possible ameliorative effect of omega-3 fish oil. Eighty (80) adult male Wistar rats weighing 180-230 gm were used. The rats were divided into eight groups containing ten (10) rats each group. Group I served as the control; Groups II, III and IV were given 5%, 20% and 40% alcohol respectively; Groups V, VI and VII were given 5% alcohol+Omega-3 fish oil; 20% alcohol+Omega-3 fish oil and 40% alcohol+Omega-3 fish oil, respectively. The Group VIII was administered Omega-3 fish oil alone. The alcohol was given at a dose of 0.005 ml/g body weight once daily using an orogastric canular. The Omega-3 fish oil was given at a dose of 0.2 ml/g body weight. Alcohol administration lasted for twelve weeks, at the end of which the rats were sacrificed by cervical dislocation. Gastric secretions were estimated, and tissues samples from the stomach collected for histomorphometric studies. The results showed that 20% alcohol caused a significant increase in gastric acid secretion when compared with the control and omega-3 only group. 40% and omega-3 group caused a decrease in gastric acid secretion when compared with the control. The histomorphometry of the stomach revealed a decrease in parietal cell and mucous cell count with increasing alcohol concentrations. Omega-3 administration showed only mild amelioration to these digestive alterations.

Effect of vagotomy on central nesfatin-1-induced decrease in gastric acid secretion

Effect of vagotomy on central nesfatin-1-induced decrease in gastric acid secretion

Gastric acid anti-secretory effects of aqueous leaf extract of Nauclea latifolia (Rubiaceae) in rats

The aqueous leaf extract of Nauclea latifolia has been shown to have anti-ulcer effect. Objectives: The present study was undertaken to investigate the effects of aqueous leaf extract of N. latifolia on gastric acid secretion as the possible mechanism of its anti-ulcer actions in male albino rats. Materials and Methods: A total of sixty (60) male albino rats were divided into two experimental studies of thirty (30) rats each. Each of the experimental studies was further divided into groups according to study design. The extract was administered orally at the doses of 100, 200 and 400 mg/kg for the experimental groups while the control and reference groups received distilled water (2 ml/kg, p.o) and cimetidine (32 mg/kg, p.o) respectively, 60 minutes prior to oral administration of indomethacin (30 mg/kg) to induce gastric mucosal injury. In the second study, gastric acid output was measured by the continuous perfusion of rat’s stomach under anesthesia with normal saline at the rate of 1 ml/min. Results: Phytochemical analysis revealed the presence of saponins, tannins, flavonoids, alkaloids and cardiac glycosides. Acute toxicity studies showed there were no deaths within 24 h after the application of the extract up to 1600 mg/kg B.W (i.p). Rats pre-treated with N. latifolia exhibited significant (P<0.05), and dose-dependent inhibition of indomethacin-induced gastric ulceration. A significant decrease in gastric acid secretion was produced by the extract at all doses studied. Conclusion: Findings of this study suggest that, aqueous extract of N. latifolia significantly reduced gastric acid secretion in indomethacin-induced gastric ulceration by inhibiting histamine-stimulated gastric acid secretion probably by occupying H2 - receptors in rats.

EFFECT OF APELIN-13 ADMINISTRATION ON GASTRIC SECRETION IN NORMAL AND DIABETIC RATS

Background: Apelin is a recently discovered peptide, identified as an endogenous ligand of receptor APJ, apelin has beneficial effect in diabetic conditions as it increase glucose uptake and improve insulin sensitivity, diabetic patients have impaired gastric secretion and apelin is expressed in parietal, chief and mucous cells and this raise the possibility of involvement of apelin in gastric physiology. Objective: The present study was carried out to demonstrate the effect of acute and chronic administration of apelin 13 on gastric secretion in normal and diabetic rats. Design: 98 adult wistar male albino rats were used, animals were divided into three main groups group A (normal rats), group B (high fat diet induced diabetic rats) and group C (streptozotocin induced diabetic rats), each group is subdivided into control subgroup (1), acute apelin-13 injected subgroup (2), chronic apelin-13 injected subgroup for 21 days (3): In all studied groups, different parameters of gastric secretion, gastric mucosal pH and mucin content were measured. Results: acute administration of apelin-13 decreased gastric acid secretion in all groups proved by significant increase in pH accompanied by significant decrease in total and free acidity, the percentage in decrease of gastric acid secretion in normal rats is more than that of high fat diet induced diabetic rats and streptozotocin induced diabetic rats. Ghrelin level, volume of gastric secretion, blood glucose and HOMA- IR significantly decreased in all groups. pepsin, mucin content of gastric mucosa and insulin level had no significant change in all groups, while, pH of gastric mucosal surface significantly increased .In addition, there was negative correlation between ghrelin level and pH, positive correlation between ghrelin and both total and free acidity in normal rats, positive correlation between ghrelin and volume of gastric secretion in all studied groups. Chronic administration of apelin-13 caused no change in gastric acidity in normal rats. and increase gastric acidity in high fat diet induced diabetic rats and streptozotocin induced diabetic rats, proved by significant decrease in pH accompanied by significant increase in total and free acidity, the percentage of increase in gastric acid secretion in high fat diet induced diabetic rats is more than that of streptozotocin induced diabetic rats, moreover, chronic administration of apelin-13decreased ghrelin level, pepsin level, volume of gastric secretion, blood glucose, insulin level and HOMA- IR and increase pH of gastric mucosal surface and mucin level in all studied groups. In addition, there is positive correlation between ghrelin and volume of gastric secretion in all studied groups. Conclusion: While apelin-13 injection on chronic run caused no change in gastric acidity in normal rats, it improved gastric acidity in diabetic rats and can act as a promising target for type 2 diabetes treatment. In addition apelin-13 can be considered as gastro protective agent as it increased pH of gastric mucosal surface and mucin level in normal and diabetic rats. Key words: Apelin, gastric secretion, diabetes.

Inhibitory effect of Canavalia gladiata extract on gastric inflammation induced by acute ethanol treatment in SD rats

We investigated the inhibitory effect of Canavalia gladiata water extract (CGW) on ethanol‐induced gastric inflammation, specifically on gastric acid secretion and gastric mucosal damage in Sprague‐Dawley (SD) rats. The possible mechanisms of CGW actions via ROS was also further determined for antioxidant effects. Rats were divided into four groups : saline(G1), gastric inflammation plus saline(G2), gastric inflammation plus Lansoprazole 30mg/kg b.w(G3), gastric inflammation plus CGW 250mg/kg b.w(G4), gastric inflammation plus CGW 500mg/kg b.w(G5). After oral administration of either saline, Lansoprazole or CGW for 7 days, acute gastric inflammation was induced by oral administration of 1mL of 70% ethanol and 0.15M HCl at groups G2,G3,G4 and G5. After 1h on ethanol administration, all animals were sacrificed. Gastric acid secretion and gastric mucosal injury were significantly decreased in G3 when compared to that of G2. And groups pretreated with CGW (G4, G5) caused a significant decrease in gastric acid secretion and gastric mucosal injury in a dose dependant manner. To examine the regulatory factors related inflammation, NF‐kB, COX‐1, COX‐2 and cytokines were measured by immuno‐histochemistry and ELISA. The expression of NF‐kB, COX‐1 and COX‐2 were clearly decreased in G3 and G5 compared with the G2. Additionally, cytokines was significantly decreased in G3 and G5. We next examined the levels of MDA and SOD activity related in antioxidative effects. Oral administration of CGW significantly decreased levels of MDA and SOD activity was dramatically increased. In conclusion, our data show that CGW has inhibitory effects on gastric inflammation induced by acute ethanol treatment in SD rat. Although the exact mechanism underlying these actions is unclear, the effects on acute gastric lesions suggest a multifactorial mechanism probably involving the antioxidant properties of CGW.

PAC1 Deficiency in a Murine Model Induces Gastric Mucosa Hypertrophy and Higher Basal Gastric Acid Output

Pituitary adenylate cyclase-activating polypeptide (PACAP) has been shown to increase the histamine release from gastric enterochromaffin-like (ECL) cells and promote gastric acid secretion in rats. In contrast, in mice, PACAP has been demonstrated to induce a decrease of gastric acid secretion, an effect presumably due to somatostatin release. To more clearly define the role of PACAP in the regulation of gastric acid output, a knockout mouse model for the PACAP-specific receptor PAC1 was applied in this study. Measurements of the basal and stimulated gastric acid secretion and morphological studies on the gastric mucosa were performed in both wild-type and PAC1-deficient mice. Compared with the wild-type mice, the PAC1-deficient mice showed a nearly threefold higher basal gastric acid output, increased gastric mucosa thickness and glands height, and proportional increases in parietal and total cell counts in the gastric mucosa. The PAC1-deficient mice also showed a trend of increased plasma gastrin levels and gastrin gene expression in the gastric mucosa. This study indicates that the expression of PAC1 is clearly important for maintaining the homeostasis of gastric acid secretion. Loss of PACAP receptor during development may lead to a compensatory mechanism regulating gastric acid secretion.

Antiulcer activity of ethanol leaf extract of Cassia fistula

The ethanol leaf extract (ELE) of Cassia fistula Linn. (Caesalpinaceae) was evaluated for antiulcer activity against pylorus ligation-induced gastric ulcer. Ranitidine (30 mg/kg b.w.) and ELE at doses of 250, 500, and 750 mg/kg b.w. were administered orally in different groups of rats (n = 6), 1 h prior to pyloric ligation. Four hours after pyloric ligation, the gastric juice was collected for evaluation of various parameters. The antiulcer activity of ELE was evidenced by the significant attenuation of gastric volume, pH, free acidity, and total acidity in the gastric juice of pyloric-ligated rats in a dose-dependent manner, and this protective effect could be due to strengthening of the mucosal defense mechanism. ELE pre-treatment significantly attenuated the fall in status of sialic acid and fucose accompanied by an increase in hexose, hexosamine, total non-amino polysaccharide, total carbohydrate, and C:P ratio in the gastric juice of pylorus-ligated rats, and this effect could be due to protection of the mucosal barrier system. ELE pre-treatment significantly prevented the increase in LPO and SOD accompanied by a fall in CAT, in the gastric juice of pyloric-ligated rats. This protective ability of ELE against pylorus ligation-induced gastric ulcer could be attributed to its free radical scavenging and antioxidant properties. Higher doses of ELE (750 mg/kg b.w.) produced maximum antiulcer activity comparable to ranitidine treatment. In essence, the antiulcer activity of ELE could be attributed to (i) a decrease in gastric acid secretion, (ii) protection of the mucosal barrier and restoration of mucosal secretions, (iii) inhibition of free radical generation or prevention of lipid peroxidation, and (iv) free radical scavenging or antioxidant properties.

Endogenous secretin in the rat--evidence for a role as an enterogastrone but failure to influence serum calcium homeostasis.

The release of secretin into plasma by intraduodenal (id) infusion of HCl or iso-osmotic (290 mosm l-1) NaCl, and the associated changes of moderately stimulated gastric acid, serum gastrin, two calciotropic hormones, total and 45calcium (Ca), were examined in the rat. The possible role of endogenous secretin as an enterogastrone and as a mediator of the hypothesized endocrine gut-thyroid-parathyroid axis was further characterized with the aid of secretin immunoneutralization and exogenous secretion. The id-HCl-stimulated secretin, measured by a sensitive radioimmunoassay, was accompanied by a decrease in gastric acid secretion, whereas secretin blockage by anti-secretin immune serum resulted in a significant increase in acid secretion. The correlation between plasma secretin and acid output was only slight. Gastrin and Ca metabolism remained unchanged during secretin stimulation. Intravenous synthetic porcine secretin at a dose reported to be effective in other target preparations (2 CU (0.58 microgram) kg-1 h-1) had no effect on gastric acid secretion and Ca metabolism. In contrast, a pharmacological dose, 32 CU (9.3 micrograms) kg-1 h-1, inhibited acid secretion, decreased serum Ca and total protein, and increased serum parathyroid hormone, but left calcitonin and gastrin unchanged. Endogenous secretin appeared to act as an enterogastrone, but whether it was the only one is unclear. No role was detected for secretin in the gut-thyroid-parathyroid axis, since the Ca changes observed may have been unspecifically mediated.

Gastroprotective effect of a traditional Chinese herbal drug “Baishouwu” on experimental gastric lesions in rats

“Baishouwu” is an appellative name of dried root tubers from three Asclepiadaceae plants: Cynanchum auriculatum Royle ex Wight, Cynanchum bungei Decne and Cynoctonum wilfordii Maxim. In order to establish the pharmacological basis for the ethnomedicinal use of Baishouwu in gastric disorders, this study examined the effects of ethanol extracts and fractions from root tubers of Cynanchum auriculatum, Cynanchum bungei and Cynoctonum wilfordii on ethanol-, indomethacin-induced gastric lesions and histamine-induced gastric acid secretion in rats. Plant materials were collected from various areas of China. Oral administration of ethanol extract and chloroform fraction of Cynoctonum wilfordii collected from Changbai Cordillera at doses of 150 and 68 mg/kg, respectively, significantly inhibited the development of ethanol- and indomethacin-induced gastric lesions and also caused significant decrease of gastric acid secretion after histamine-induced gastric lesion. Oral administrations of ethanol extract and chloroform fraction of Cynanchum auriculatum collected from Binhai at the doses of 300 and 69 mg/kg, respectively, significantly inhibited ethanol- and indomethacin-induced gastric lesions. This study demonstrates the gastroprotective property of Baishouwu for the first time.

Insulin-like growth factor I accelerates gastric ulcer healing by stimulating cell proliferation and by inhibiting gastric acid secretion.

Given the importance of Insulin-Like Growth Factor I (IGF-I) to intestinal maintenance and the presence of IGF-I in salivary glands, we hypothesized that IGF-I participates in the healing of gastric ulcers. The aim of the study was to determine: 1) whether IGF-I applied locally would support gastric ulcer healing by increasing cell proliferation and 2) the effect of IGF-I on gastric acid secretion. Gastric ulcers were induced with a cryoprobe. Immediately thereafter, IGF-I (0.4, 4.0 and 40 microg) or vehicle was infiltrated perifocally. In another group, animals received a daily dose of 40 micromol omeprazole subcutaneously. Ulcer healing was evaluated by ulcer size and histological examination at 7 days. Pentagastrin-stimulated gastric acid secretion was evaluated in conscious rats with gastric fistula, after IGF-I (400 microg) had been injected intravenously. IGF-I significantly reduced ulcer size, but only at low doses (0.4 microg/kg body weight (BW), P = 0.008; 4 microg/kg BW, P = 0.001). This effect was similar to omeprazole treatment. Histological examination after IGF-I administration showed increased cell proliferation, increased IGF-I content and down-regulated IGF-I receptors. The secretory studies demonstrated a significant decrease in gastric acid secretion 30 min after IGF-I bolus injection (IGF-I: 53 +/- 11 microEq; vehicle: 116 +/- 5 microEq; P=0.001), which lasted for more than 1 h. IGF-I stimulates gastric ulcer healing, stimulating cell proliferation and inhibiting gastric acid secretion.

Atropine-induced gastrointestinal cytoprotection dependences to the intact of vagal nerve against indomethacin-induced gastrointestinal mucosal and microvascular damage in rats

The non-steroidal antiinflammatory drugs, such as an indomethacin (IND), cause mucosal ulceration and increase the mucosal vascular permeability in the gastrointestinal (GI) tract. Some exogenous agents, e.g. the atropine, can protect the GI mucosa against these ulcerogenic effects. The gastrointestinal functions and mucosal protection, however, are regulated by the vagal nerve. The aims of this study was to examine the dependence of atropine-induced GI cytoprotection to the vagal innervation against the development of IND-caused ulcers and microvascular damage in the mucosa of stomach and small intestine in rats. Methods: the observations were carried out on CFY-strain rats. The mucosal damage was produced by subcutaneous administration of IND in a 20 mg/kg dose 24 h prior to the killing of animals at the same time as the start of atropine-application, which was given in a small dose (0.1 mg/kg) every 5 h. The subdiaphragmatic bilateral surgical vagotomy was done 24 h before the experiment. The vascular permeability, indicated by the microvascular endothel damage, was measured by the appearance and concentration of intravenously administered Evans blue into the GI mucosa. The number and severity of mucosal lesions and the Evans blue content of mucosa were determined in the stomach and small intestine. Results: (1) The IND caused mucosal ulcers and Evans blue extravasation into the mucosa of the stomach and small intestine. (2) The IND-induced mucosal ulceration and vascular permeability significantly decreased after atropine-administartion in the same parts of GI tract. (3) The extent of cytoprotective effect of atropine against the IND was decreased after bilateral surgical vagotomy. Conclusions: (1) The IND causes microvascular endothel damage in the stomach and small intestinal. (2) The atropine has a cytoprotective effect in the stomach and small intestine against the aggressive effects of IND without decrease of gastric acid secretion. (3) The intact vagal nerve is necessary to the function of cytoprotective mechanisms of atropine against the IND.

Anti-Diarrhegenic and Anti-Ulcer Properties of Irvingia gabonensis in Rats

The crude methanol extract of Irvingia gabonensis was evaluated for effects on gastrointestinal motility and indomethacin-induced gastric ulceration. The extract (50, 100 and 200 mg/kg, p.o.) exhibited dose-dependent inhibition of indomethacin-induced gastric ulceration that seems to be stronger than cimetidine (50 mg/kg). A significant decrease in gastric acid secretion with concomitant increase in intragastric mucous secretion was produced by the extract at all doses studied. Gastrointestinal motility was significantly reduced in the extract-treated rats. Acute toxicity studies showed there were no deaths either 24 h or 7 days after the application of the extract up to 1600 mg/kg. The results show that Irvingia gabonensis possesses anti-diarrhegenic and anti-ulcer properties. The anti-ulcer property probably act via a reduction in gastric acid secretion and an increase in the intragastric mucous secretion.

Helicobacter pylori infection is a major risk factor in the decrease of gastric acid secretion in the elderly

Helicobacter pylori infection is a major risk factor in the decrease of gastric acid secretion in the elderly

Effects of TRH on gastric acid secretion: A model for human study

The possible effects of TRH administration on different parameters of gastric function were studied in 10 patients with different gastrointestinal complaints. Basal (BAO) and pentagastrin stimulated (6 μg pentagastrin/kg bw sc) maximal (MAO) acid output were determined and serum levels of TSH, total and free thyroxine (T4 and FT4), triiodothyronine (T3) were measured. After determinations of BAO and MAO and the hormones indicated above, one group of patients received a TRH injection (0.2 mg protirelin) intravenously. The second group of patients was injected with atropine (atropinum sulfuricum, 1 mg, iv). At different times following the injections in both groups of patients BAO, MAO and serum levels of TSH, total and free T4, T3, gastrin were determined. Injection of TRH resulted in an increase in TSH and with some delay in thyroxine and gastric acid levels. Atropine treatment was followed by a decrease in gastric acid secretion and a small decrease in TSH and no changes in the values of the other studied hormones. The results suggest a complex interrelationship between TRH, vagal system and pentagastrin-dependent gastric acid secretion operating in human subjects.

Effects of intravenous vasoactive intestinal peptide injection on jejunal alanine absorption and gastric acid secretion in rats

The effect of intravenous vasoactive intestinal polypeptide (VIP) injection on jejunal l-alanine absorption and gastric acid secretion in the rat was investigated. Continuous intravenous VIP infusion (11.2 ng/kg per min) throughout the experimental period (160 min) produced 60% decrease in alanine absorption and 40% decrease in gastric acid secretion during the second hour of the experiment. Subdiaphragmatic vagotomy reduced alanine absorption to 91% ( P>0.05) and 71.3% ( P<0.05) of control value during the first and second hours of perfusion, respectively. VIP infusion following vagotomy elicited a reduced effect when compared to that produced by similar injections in normal rats. Gastric secretion in vagotomized rats was reduced by 40% ( P<0.05) below control. VIP infusion in vagotomized rats exerted a significant decrease ( P<0.05) of gastric acid secretion. Moreover, water absorption was decreased by almost 10% ( P<0.05) after i.v. injection of VIP and was increased by 20–24% above control value following vagotomy. However, i.v. administration of VIP following vagotomy did not elicit any further change in water absorption. It can be concluded that VIP inhibits alanine absorption and gastric acid secretion in the rat and that these inhibitory effects might be partially mediated by the vagus nerve.

Gastric adaptation to stress: role of sensory nerves, salivary glands, and adrenal glands.

Single exposure to water immersion and restraint stress (WRS) in rats produces acute gastric mucosal damage, but repetitive WRS insults lead to gastric adaptation to stress ulcerogenesis. This study was designed to assess the mechanism of this adaptation, particularly the role of sensory nerves, salivary glands, adrenal glands, and gastric acid secretion. WRS was applied for a standard period of 3.5 h, either once or repeated every other day for up to 8 days in intact rats and in animals with capsaicin-induced deactivation of sensory nerves, vagotomy, salivectomy, adrenalectomy, and inhibition of gastric acid secretion by H2-blocker. WRS applied once produced multiple gastric erosions accompanied by a significant increase in gastric acid secretion and a decrease in gastric blood flow (GBF) and DNA synthesis. Repeated WRS insults resulted in a significant decrease in the number of gastric lesions, reaching a maximum after four consecutive exposures to WRS. This adaptation to stress ulcerogenesis was accompanied by a decrease in gastric acid secretion and an increase in GBF and mucosal generation of DNA synthesis. Salivectomy, which decreased the luminal content of epidermal growth factor (EGF) (by about 80%), markedly attenuated this adaptation, and this was reversed by the addition of exogenous EGF. Capsaicin-induced ablation of sensory nerves eliminated gastric adaptation to WRS, and this was accompanied by a significant decrease in the GBF, but pretreatment with calcitonin gene-related peptide restored gastric adaptation to stress in capsaicin-denervated rats. Selective vagotomy and adrenalectomy failed to affect gastric adaptation to WRS, whereas gastric acid inhibition by ranitidine enhanced this adaptation. The stomach is able to adapt to repeated stress insults by enhancing GBF and DNA synthesis, and this adaptation is mediated, at least in part, by sensory nerves and EGF.