Gastric Pepsin Secretion Research Articles

Evaluation of Hydro-alcoholic extract of Corchorus capsularis seeds for its Anti-ulcer activity on Albino Wistar Rat

The objective of present study was to evaluate the anti-ulcer activity of hydro-alcoholic extract of Corchorus capsularis seeds. Mainly hyper secretion of gastric acid and pepsin causes ulcer in patients. Plant extracts and polyherbal formulations are two of the most appealing sources of new drug. This type of extract formulations are showing good results in the treatment of gastric ulcers. In this study anti-ulcer activity was investigated by pyloric ligation, aspirin and stress induced gastric ulcer in albino wistar rats. The extract was given at the dose of 250mg/kg (CCLD- Corchorus capsularis low dose) and 500mg/kg (CCHD- Corchorus capsularis high dose) in all the experimental models. Ranitidine (150mg/kg) was used as standard drug. CCLD and CCHD showed 37.49% and 63.14% ulcer inhibition respectively, whereas ranitidine 69.69% against pylorus ligation induced ulcer. In aspirin induced ulcer model the extract showed ulcer inhibition 48.64% and 64.00% in CCLD and CCHD respectively whereas the standard drug ranitidine exhibited 84.64% ulcer inhibition. In stress induced ulcer model CCLD, CCHD and ranitidine exhibited 48.64%, 64.00% and 84.64% ulcer inhibition respectively. In all the models ethanolic extract of Corchorus capsularis seeds has shown significant anti-ulcer activity in dose dependent manner.

Peptic ulcer disease

Peptic ulcer disease (PUD) is defined as a disruption in the innermost lining of the gastrointestinal tract, due to the secretion of gastric acid or pepsin. The disruption is in the gastric epithelial layer, specifically the muscularis mucosae. PUD normally affects the stomach along with the first and second parts of the duodenum, although it is not limited to these areas. Typically, gastric ulcers induce upper abdominal pain within 30 minutes of eating, whereas duodenal ulcers cause discomfort much later. Endoscopic and histological investigations are the key to early identification and treatment of patients with PUD, with testing for Helicobacter pylori necessary in those patients suspected of having PUD. In this article we will be looking at the aetiology, pathophysiology and management of PUD.

Gastroprotective Effect of Green Algae Extract (Ulva lactuca L) on Gastric Rats

Gastric ulcer is a disease of the digestive tract characterized by mucous damage to secretion of gastric acid and pepsin. One of the potential gastroprotector plants is green algae. The purpose of this study was to examine the gastroprotective effect of ethanol extract of green algae (EEGH) Ulva lactuca L on the gastric of ethanol-induced rats. This study used 36 rats, divided into 6 groups. Group I is a normal group. Group II negative control, ethanol 96% induced. Group III positive control, given comparison of ranitidine dose of 15.75 mg/kgBW. Groups IV, V and VI were given multilevel EEGH, namely 125, 250 and 500 mg/kgBW. The treatment was carried out for 14 days, on the 14th day ethanol 96% was induced and then dissected. Research data on gastric ulcer index and protection ratio were analyzed using One Way ANOVA with a confidence level of 95%. The results of the EEGH statistical test dose of 500 mg/kgBW with negative controls showed a significant difference with p value of 0.013 (p<0.05). The EEGH 500 mg/kgBW has the ability as an effective gastroprotector, as seen from the gastric ulcer index value of 0.5 and the protection ratio of 78.94%.Keywords: Ethanol, gastroprotector, protection ratio, ulcer index, Ulva lactuca L.78,94%.

Molecular mechanisms of Wischnewski spot development on gastric mucosa in fatal hypothermia: an experimental study in rats

Numerous dark-brown-coloured small spots called “Wischnewski spots” are often observed in the gastric mucosa in the patients dying of hypothermia, but the molecular mechanisms through which they develop remain unclear. We hypothesised that hypothermia may activate the secretion of gastric acid and pepsin, leading to the development of the spots. To investigate this, we performed experiments using organotypic rat gastric tissue slices cultured at 37 °C (control) or 32 °C (cold). Cold loading for 6 h lowered the extracellular pH in the culture medium. The mRNA expression of gastrin, which regulates gastric acid secretion, increased after cold loading for 3 h. Cold loading increased the expression of gastric H+,K+-ATPase pump protein in the apical canalicular membrane and resulted in dynamic morphological changes in parietal cells. Cold loading resulted in an increased abundance of pepsin C protein and an elevated mRNA expression of its precursor progastricsin. Collectively, our findings clarified that cold stress induces acidification by activating gastric H+,K+-ATPase pumps and promoting pepsin C release through inducing progastricsin expression on the gastric mucosa, leading to tiny haemorrhages or erosions of the gastric mucosa that manifest as Wischnewski spots in fatal hypothermia.

Association of Helicobacter pylori infection and vitamin B12 deficiency

H. pylori infection is strongly related with chronic gastritis of the stomach, which causes impairment in gastric acid and secretion of pepsin, and linked to male absorption of food-vitamin B12. The most important virulence genes accompanying stomach and intestine disease are (cag A and vac A). Aim of the study: To evaluate the rate of gastric ulcer infection with H. pylori and its detect CagA gene in H.pylori isolated from gastritis. Materials and Methods: A total of 200 biopsy patients aged from (10- ≥ 60) years were collected from Baqubah teaching hospitals. They were suffering from gastric upset and attended to endoscopic unit of department of medicine. Questioners including, sex, age, smoking, presence of cancer, and biopsies of gastric tissue were collected from the corpus or the ant rum or corpus and ant rum of the patient's stomach. Three biopsies were taken from each patient. Histopathologic study, gram staining, and rapid urease test working for each patients. Serology Test Serum Enzyme-Linked Immunosorbent Assay Testing (ELISA).

Esomeprazole alleviates the damage to stress ulcer in rats through not only its antisecretory effect but its antioxidant effect by inactivating the p38 MAPK and NF-κB signaling pathways.

BackgroundStress ulcer is a severe complication in critically ill patients and causes a high mortality. The proton pump inhibitor esomeprazole is widely applied in the treatment of stress ulcers because of its powerful acid suppression ability. However, the mechanism of stress ulcer and the precise gastroprotective effect of esomeprazole in stress ulcer remain unclear.PurposeIn the present study, the rats with water-immersed and restraint (WIR)-induced stress ulcer were used to further elucidate the anti-ulcerogenic capacity of esomeprazole in stress ulcer in addition to its anti-acid secreting ability.Methods and resultsThe rats were randomly divided into 5 groups: control group (NS), water-immersed and restraint group (WIR), high-dose application of esomeprazole plus stress ulcer-induced group (HE+WIR), low-dose application of esomeprazole plus stress ulcer-induced group (LE+WIR), and high-dose application of esomeprazole without stress ulcer-induced group (HE). Our study showed that the pretreatment of esomeprazole alleviated gastric tissue damage in both macroscopic and histopathological manifestations. Pretreatment of esomeprazole elevated the decline in PEG2 level affected by WIR; and it inhibited the secretion of gastric acid, gastrin and pepsin. Moreover, esomeprazole exerted its antioxidant effects by reducing malondialdehyde levels, enhancing the expressions of antioxidant factors like glutathione and superoxide dismutase (SOD) and reducing the compensatory transcriptional elevation of SOD1 gene. Esomeprazole also reduced the levels of MPO (myeloperoxidase), tumor necrosis factor (TNF)-α and interleukin (IL)-1β according to its anti-inflammatory effects. We further explored the possible mechanism of esomeprazole pretreatment on stress ulcer and demonstrated that esomeprazole attenuated the high phosphorylation levels of nuclear factor kappa B (NF-κB) p65 and p38 MAPK, and decreased the NF-κB p65 nuclear translocation induced by WIR related stress ulcer.ConclusionOur study provides some evidence that the esomeprazole pretreatment exerts gastroprotective effects in WIR-induced stress ulcer through not only its antisecretory effect but also its antioxidant effect by inactivating the p38 MAPK and NF-κB signaling pathways.

Vitamin B12 Deficiency in Helicobacter pylori Infected Patients

Background: H. pylori infection is strongly related with chronic gastritis of the antrum of the stomach, which causes impairment in gastric acid and pepsin secretion, and is thus linked to malabsorption of food-vitamin B12. H. pylori can cause an individual to have a vitamin B12 deficiency. It is also a known contributor to gastritis ulcers and it can prevent the stomach from being able to absorb the vitamin B12 you consume and leads to a deficiency of vitamin B12. The purpose of this study is to determine the frequency of vitamin B12 deficiency in Helicobacter pylori infected patients. Methods: All patients aged 17 - 65 years, of either gender were evaluated for urine vitamin B12 level by human vitamin B12 ElSA kit. The data were analyzed in statistical software (SPSS) and the P-value = 0.05 was considered as statistically significant. Results: Of one hundred subjects, 65 (65%) were males, while 35 (35%) were females. 31 (36.0%) H. pylori infected patients had normal vitamin B12 level and 55 (64%) were Vitamin B12 deficiency in 86 (86%). H. pylori infected patients with a significant difference (P value Helicobacter pylori infected patients.

Effects of Ramadan Fasting on Common Upper Gastrointestinal Disorders: A Review of the Literature

Introduction: Ramadan is the ninth month of Muslim's calendar during which Muslims fast. Ramadan lasts 29-30 days based on the visual sightings of the crescent moon. Fasting during Ramadan has significant health effects. The present study aimed at reviewing the literature of the impact of Ramadan fasting on upper gastrointestinal disorders. Methods: MEDLINE and Google Scholar were searched by using ((“Ramadan” R fasting”) AND( Upper Tract OR Gastrointestinal Diseases OR Dyspepsia OR Gastroesophageal Reflux OR Peptic Ulcer OR Gastrointestinal Hemorrhage)) as keywords in the title and abstract. Relevant, non- duplicate full articles written in English were reviewed. Results: Gastric acid and pepsin secretion increase during Ramadan fasting, probably associated with dyspeptic symptoms. Regarding peptic ulcer frequency, results are inconsistent. However, peptic ulcer complications such as gastrointestinal bleeding and peptic ulcer perforation increase during Ramadan fasting. Conclusion: Fasting during Ramadan seems to be beneficial for healthy individuals, but in people with gastrointestinal disorders, it might be harmful as it increases the risk of complications. Therefore, taking medical advice before Ramadan fasting is highly recommended to people suffering from gastrointestinal symptoms.

Potential of in vivo real-time gastric gas profiling: a pilot evaluation of heat-stress and modulating dietary cinnamon effect in an animal model.

Gastroenterologists are still unable to differentiate between some of the most ordinary disorders of the gut and consequently patients are misdiagnosed. We have developed a swallowable gas sensor capsule for addressing this. The gases of the gut are the by-product of the fermentation processes during digestion, affected by the gut state and can consequently provide the needed information regarding the health of the gut. Here we present the first study on gas sensor capsules for revealing the effect of a medical supplement in an animal (pig) model. We characterise the real-time alterations of gastric-gas in response to environmental heat-stress and dietary cinnamon and use the gas profiles for understanding the bio-physiological changes. Under no heat-stress, feeding increases gastric CO2 concentration, while dietary cinnamon reduces it due to decrease in gastric acid and pepsin secretion. Alternatively, heat-stress leads to hyperventilation in pigs, which reduces CO2 concentration and with the cinnamon treatment, CO2 diminishes even more, resulting in health improvement outcomes. Overall, a good repeatability in gas profiles is also observed. The model demonstrates the strong potential of real-time gas profiler in providing new physiological information that will impact understanding of therapeutics, presenting a highly reliable device for monitoring/diagnostics of gastrointestinal disorders.

Gastric ulceration: the role of thermoxidized palm oil

Purpose– The purpose of this paper is to study the effect of chronic consumption of fresh palm oil (FPO) and thermoxidized palm oil (TPO) diet on gastric acid secretion, pepsin secretions, gastric mucus output and gastric cytoprotection.Design/methodology/approach– Adult Wistar rats were randomly assigned into three groups, i.e. control, FPO and TPO groups (n= 10 in each). The control group was fed with normal rat chow only, the FPO group was fed on diet containing 15 per cent v/w FPO and the TPO group was fed with diet containing v/w of thermally oxidized palm oil. All animals had free access to feed and water, and the feeding lasted for 14 weeks. At the end of the feeding period, gastric acid secretion, pepsin secretion, mucus output and gastric ulceration were measured following standard methods.Findings– There was increase in histamine-stimulated gastric acid output in the TPO diet-fed group (p< 0.01) compared with the control and FPO diet-fed groups. No significant change in the mucus output was observed across all the experimental groups; whereas, pepsin secretion was significantly higher (p< 0.05) in the TPO diet-fed group (0.46 ± 0.27) compared with the control (0.14 ± 0.05) and FPO diet-fed groups (0.25 ± 0.01). Ulcer scores in the TPO diet-fed group (15.5 ± 0.33) was significantly higher (p< 0.01) compared with the control (10.0 ± 0.05) and FPO diet-fed (5.0 ± 0.04) groups.Originality/value– Chronic consumption of TPO increased gastric acid and pepsin secretion (gastric-aggressive factors) without a change in the mucus output. This can bring about gastric ulceration; therefore, the liberal use of TPO should be discouraged.

Effect of Cannabis sativa extract on gastric acid secretion, oxidative stress and gastric mucosal integrity in rats

Studies were conducted in pylorus-ligated rats to investigate the effect of Cannabis sativa extract on gastric acid secretion, experimental gastric ulcer and on oxidative stress and inflammatory markers in the gastric mucosa. C. sativa (5, 10 and 20 mg/kg, expressed as Δ9-tetrahydrocannabinol) was administered subcutaneously daily for 4 weeks prior to pylorus ligation and different treatments. Under basal conditions, pretreatment with cannabis extract at doses of 5 and 10 mg/kg increased gastric acid secretion and induced minimally visible gastric mucosal lesions in the 4 h pylorus-ligated rat. Malondialdehyde and nitric acid concentration increased, while reduced glutathione decreased by cannabis at doses of 5 and 10 mg/kg in gastric mucosa. TNF-α increased by cannabis extract at doses of 5 and 10 mg/kg but decreased following the high dose of 20 mg/kg. On the other hand, the gastric acid secretory responses stimulated by pentagastrin or carbachol (but not histamine) were inhibited in rats pretreated with cannabis extract. Under these conditions, cannabis decreased pepsin content after pentagastrin and carbachol but not histamine stimulation. Cannabis also decreased lipid peroxidation and nitric oxide content, and increased both reduced glutathione and catalase activity in mucosa. Moreover, cannabis decreased mucosal inflammation (level of TNF-α) and the development of gastric mucosal lesions. Cannabis administered for 1 month prior to pylorus-ligation and either acidified aspirin or ethanol (96 %) decreased the development of gastric mucosal damage in a dose-dependent manner, along with reduction in gastric acid output, gastric mucosal oxidative stress and inflammation (TNF-α). Sections of gastric mucosa stained with periodic acid Schiff showed increased mucus secretion by cannabis in basal conditions and after treatment with aspirin or ethanol. Results indicate that: (1) the effect of cannabis differs in basal conditions and after exposure of the gastric mucosa to high acid concentrations or other chemical noxious agents; (2) cannabis administered systemically exerts gastric mucosal protective effects against mucosal damage evoked by stimulation of gastric acid secretion, acidified aspirin or ethanol. These effects of cannabis are likely to involve inhibition of gastric acid and pepsin secretion, increased mucus, decreased oxidative stress and inflammation in gastric mucosa.

Anti-ulcerogenic activity of aqueous extract of Carica papaya seed on indomethacin-induced peptic ulcer in male albino rats

ObjectiveCarica papaya is an important fruit with its seeds used in the treatment of ulcer in Nigeria. This study investigated the anti-ulcerogenic and antioxidant activities of aqueous extract of Carica papaya seed against indomethacin-induced peptic ulcer in male rats. MethodsThirty male rats were separated into 6 groups (A–F) of five rats each. For 14 d before ulcer induction with indomethacin, groups received once daily oral doses of vehicle (distilled water), cimetidine 200 mg/kg body weight (BW), or aqueous extract of C. papaya seed at doses of 100, 150 or 200 mg/kg BW (groups A, B, C, D, E and F, respectively). Twenty-four hours after the last treatment, groups B, C, D, E and F were treated with 100 mg/kg BW of indomethacin to induce ulcer formation. ResultsCarica papaya seed extract significantly (P<0.05) increased gastric pH and percentage of ulcer inhibition relative to indomethacin-induced ulcer rats. The extract significantly (P<0.05) decreased gastric acidity, gastric acid output, gastric pepsin secretion, ulcer index and gastric secretion volume relative to group B. These results were similar to that achieved by pretreatment with cimetidine. Specific activities of superoxide dismutase, catalase, glutathione peroxidase, glutathione reductase and glucose-6-phosphate dehydrogenase in the extract-treated groups (D, E and F) were increased significantly over the group B (P<0.05). Pretreatment with the seed extract protected rats from the indomethacin-mediated decrease in enzyme function experienced by the group B. Similarly, indomethacin-mediated decrease in reduced glutathione level and indomethacin-mediated increase in malondialdehyde were reversed by Carica papaya extract. ConclusionIn this study, pretreatment with aqueous extract of Carica papaya seed exhibited anti-ulcerogenic and antioxidant effects, which may be due to the enhanced antioxidant enzymes.

Identification of Vitamin B12 Deficiency in Helicobacter pylori Infected Patients

Background: H. pylori infection is strongly related with chronic gastritis of the antrum of the stomach, which causes impairment in gastric acid and pepsin secretion, and is thus linked to malabsorption of food-vitamin B12. H. pylori can cause an individual to have a vitamin B12 deficiency. It is also a known contributor to gastritis ulcers and it can prevent to the stomach from being able to absorb the vitamin B12 you consume and leads to a deficiency of vitamin B12. The purpose of this study is to determine the frequency of vitamin B12 deficiency in Helicobacter pylori infected patients. Methods: All patients above 13 years of age, of either gender with Helicobacter pylori infection were evaluated for urine vitamin B12 level by human vitamin B12 ElSA kit. The data was analyzed in statistical software (SPSS) and the P-value=0.05 was considered as statistically significant. Results: One hundred and twenty nine (129) Helicobacter pylori infected patients with means age 44.3176 ± 15.9114 (males) and 49.6308 ± 15.1612 (females) were enrolled and evaluated. Sixty seven (52%) H. pylori infected patients had normal vitamin B12 level, 31 (47%) were males and 36 (53%) were females. Whereas sixty tow (48%) H. pylori infected patient had low vitamin B12 level, 42 (67%) were males and 20 (33%) were females with (p-value 0.02). Conclusions: The frequency of vitamin B12 deficiency observed in H. pylori infected patients in this study (48%). However, there is a significant difference between H. pylori infected male patients and female patients who had deficient in vitamin B12 (68%, 32% respectively) with p value (0.01*).

Вплив низькомолекулярної органічної сполуки 2-(2-гідроксифенокси)ацетил)-L-пролінат натрію на стимульовану карбахоліном шлункову секрецію у щурів

Тto investigate the effects of low molecular organic compound (LMOC) on gastric acid secretion (GAS), pepsin output and the activity of Н+,К+-ATPase in the conditions of carbachol stimulation. GAS stimulated by carbachol was measured by method of isolated perfused stomach, pepsin output was analyzed by colorimetric method for 120 minutes and the activity of Н+,К+-ATPase was assessed spectrophotometrically by the level of anorganic phosphate on 20 white laboratory rats. GAS, pepsin output and the Н+,К+-ATPase activity were decreased under the carbachol stimulation after injection of LMOC. LMOC decreases the gastric acid and pepsin secretion in terms of carbachol stimulation. The inhibition of Н+,К+-ATPase activity is considered as mechanism of antisecretory property of LMOC.

Ulcerogenic and intestinal motility/transit stimulating actions of nevirapine in albino Wistar rats

The antiretroviral is a non-nucleoside reverse transcriptase inhibitor of human immunodeficiency virus type 1. This study was undertaken to investigate the effect of nevirapine (NVP) administration on gastric acid secretion, pepsin secretion, mucosal secretion, intestinal motility, and transit using apparently healthy albino Wistar rats. Eighty albino Wistar rats (50-125 g body weight) from the start of the experiment were used for the study. Rats in the control group were fed normal rodent chow, while the NVP group was fed by gavage NVP (0.4 mg/kg body weight) two times daily (07:00 and 18:00 hours) in addition to normal rodent chow for 12 weeks. All animals were allowed free access to clean drinking water. Mean basal gastric output and peak acid output following histamine administration in the NVP-treated group were significantly higher (p < 0.001, respectively) compared to the control. Following cimetidine administration, there was significant decrease (p < 0.001) in peak acid output in the NVP-treated group compared to the control. The concentration of gastric pepsin, adherent mucus secretion, and mean value for ulcer score were significantly higher (p < 0.001) compared to their control group, respectively. There were significant increases (p < 0.05, respectively) in intestinal motility and basal contraction (p < 0.05) and increase in intestinal transit of the ileum of NVP-treated rats compared to their control, respectively. Results of the study suggest that NVP administration might provoke gastric ulceration in rats which may be caused by high pepsin, high basal acid output, and increased intestinal motility and transit.

Influence of aging on experimental gastrointestinal motility in extraction of rat molar teeth

The purpose of the present study was to determine whether different consistency of diet and malocclusion induced by the extraction of molar teeth on the masticatory organs modulated gastric acid secretion, gastric emptying and intestinal transit in young and elder rats. Male Wistar rats (young, 5 weeks; elder, 1.5 years) were used in this experiment, and were divided into 2 groups. Group one (G1) was maintained with solid diet, Group two (G2) with mud diet. Further, the mandibular molar teeth of G2 were extracted. The experimental period was 10 weeks. The effect of aging and malocclusion on the parameters of gastric secretion was examined using pylorus-ligated rats. The gastric emptying rate (GER) and small intestinal transit rate was determined in rats by evans blue from the stomach and charcoal from the small intestinal, respectively. In pylorus-ligated rats, Young-G2 rat of gastric juice volume, acid output and pepsin secretion remarkably showed significant decrease in comparison with Young-G1 group, but there was not significant difference between Elder-G1 and Elder-G2. GER of Young-G2 rat group was 44.2±7.9%, significantly lower than that of Young-G1 rat group (61.6±8.8%, P <0.01), but Elder-G1 rat group were not significantly different than those of rats of Elder-G2 group. In small intestinal transit rates of charcoal meals, G1 and G2 of young were 73.3±9.1 and 55.1±8.6%, respectively, and Elder groups were 61.7±9.8 and 52.6±7.7%, suggesting an insignificant effect on diet. These results suggest that the diet and malocclusion, induced by extraction of mandibular molar teeth of young rat groups, may have a great influence compared to elder rat groups.

Effect of Mica Monomer Powder on Chief and Parietal Cells as well as G and D Cells in Gastric Mucosa of Chronic Atrophic Gastritis in Rats

To study the regulative action of mica monomer powder preparation on the chief and parietal cells as well as G and D cells in the gastric mucosa of the experimental atrophic gastritis (CAG) rats. Intervention therapy was given to the experimental CAG rats at three different doses of mica monomer powder preparation to evaluate the changes of chief and parietal cells as well as G and D cells in the gastric mucosa and the histopathological changes of gastric mucosa. Mica monomer powder preparation at three different doses could increase the amount of chief and parietal cells as well as G and D cells in gastric mucosa of the experimental CAG rats and alleviate and control the inflammation of gastric mucosa and the atrophy of gastric mucosa glands. Especially, better effects were shown in the mid and high dose groups. Mica has the pharmacological action of protecting the gastric mucosa, enhancing blood flow of the gastric mucosa, and consequently improving the inflammatory responses of the gastric mucosa. One of the mechanisms is associated with promoting the secretion of gastric acid and gastric pepsin and regulating the neuroendocrine mechanism including gut hormone secretion (gastrin and somatostatin) by increasing the number of chief and parietal cells as well as G and D cells.

Effects of cysteamine on in vitro maturation of mouse oocytes (IVM) in two media

and pepsin secretions were measured by titration and the Anson method, respectively. Stages of the measurements were basal (first and second), stimulated and returnedbasal. Results: Basal acid and pepsin secretions in the paraoxon group (14.61± 1.46 and 2.97± 0.32 g/15 min, respectively) were more than those in the control group (7.88± 0.26 and 0.55± 0.06 mol/15 min). Although pentagastrinstimulated acid secretion in all the three groups was more than basal acid secretion, there were no differences between the groups. Stimulated pepsin secretion in the paraoxon group was significantly more than that in the control group. Conclusion: Paraoxon, in chronic exposure, increases gastric acid and pepsin secretion.

The effect of chronic consumption of paraoxon on basal and pentagastrin-stimulated gastric acid and pepsin secretion in rats

The effect of chronic consumption of paraoxon on basal and pentagastrin-stimulated gastric acid and pepsin secretion in rats

The effect of acute consumption of paraoxon on basal and pentagastrin-stimulated gastric acid and pepsin secretion in rats

The effect of acute consumption of paraoxon on basal and pentagastrin-stimulated gastric acid and pepsin secretion in rats