Naloxone or Vagotomy Does Not Influence Centrally Octreotide-induced Inhibition of Gastric Acid Secretion in Rats

Summary： To investigate the effect of preceding naloxone injection into the third cerebroventricle or acute subdiaphragmatic vagotomy on the gastric acid secretion inhibited by the somatostatin analogue octreotide given by intracerebroventricular （icv） injection. The third ventricles were cannulated in male Wistar rats anesthetized with sodium pentobarbital. One week later, acute gastric lumen perfusion was carried out. The gastric perfusion samples were collected every 10 min and were titrated by 0.01 mol/L NaOH to neuter. On the basis of subcutaneous injection of pentagastrin （G-5, 160 g/kg）, icv injection of physiological saline （group A, n=20）, icv injection of octreotide （0.05 μ g） （group B, n=20）, icv injection of naloxone （2.5 μ g）＋octreotide （0.05 μg） （group C, n=20）, acute subdiaphragmatic vagotomy＋ icv injection of physiological saline （group D, n=20）, or acute subdia- phragrnatic vagotomy＋icv injection of octreotide （0.05 μg） （group E, n=20） were conducted. Before and after icv injection, 1-h total acid output （TAO） was determined and compared. The experimental data were expressed in change rate （%） of TAO. The change rates （%） of TAO were 4.60 % in group A, -20.35 % in group B, - 18.06 % in group C, 5.01% in group D and -21.59 % in group E, respectively. Comparison of group B or C versus group A showed that P〈0.01 and comparison between the group E versus group D showed that P〈0.01. Whereas the differences between group C and group B, group E and group B were not statistically significant （P〉0.05 for all）. The results indicate that the central inhibition of gastric acid secretion by octreotide may not be mediated by the endogenous opi- ate substance or its receptor and the peripheral pathway for icv injection of octreotide to suppress gastric acid secretion is via extra-vagus route.

Helicobacter pylori eradication to prevent gastric cancer: underlying molecular and cellular mechanisms

Numerous cellular and molecular events have been described in development of gastric cancer. In this artide, we overviewed roles of Helicobacter pylori （H pylori） infection on some of the important events in gastric carcinogenesis and discussed whether these cellular and molecular events are reversible after cure of the infection. There are several bacterial components affecting gastric epithelial kinetics and promotion of gastric carcinogenesis. The bacterium also increases risks of genetic instability and mutations due to NO and other reactive oxygen species. Epigenetic silencing of tumor suppressor genes such as RUNX3 may alter the frequency of phenotype change of gastric glands to those with intestinal metaplasia. Host factors such as increased expression of growth factors, cytokines and COX-2 have been also reported in non-cancerous tissue in Hpylori-positive subjects. It is noteworthy that most of the above phenomena are reversed after the cure of the infection. However, some of them including overexpression of COX-2 continue to exist and may increase risks for carcinogenesis in metaplastic or dysplastic mucosa even after successful H pylori eradication. Thus, H pylori eradication may not completely abolish the risk for gastric carcinogenesis. Efficiency of the cure of the infection in suppressing gastric cancer depends on the timing and the target population, and warrant further investigation.

Reduced gastric acid production in burn shock period and its significance in the prevention and treatment of acute gastric mucosal lesions

AIM To investigate the changes of gastric acidproduction and its mechanism in shock period ofsevere burn in rats.METHODS A rat model with 30% TBSA full-thickness burn injury was employed and thegastric acid production,together with gastricmucosal blood flow(GMBF)and energy charge(EC)were measured serially within 48hpostburn.RESULTS The gastric acid production in theacute shock period was markedly inhibited aftersevere burn injury.At the 3rd h postburn,thegastric juice volume,total acidity and acidoutput were already significantly decreased(P【0.01),and reached the lowest point,0.63mL/L±0.20mL/L,10.81mmol/L±2.58mmol/L and 2.23mmol/h±0.73mmol/hrespectively,at the 12th h postburn.Althoughrestored to some degree 24 h after thermalinjury,the variables above were stillstatistically lower,compared with those ofcontrol animals at the 48th h postburn.TheGMBF and EC were also significantly reducedafter severe burns,consistent with the trend ofgastric acid production changes.CONCLUSION Gastric acid production,as wellas GMBF and EC was predominantly decreased in the early postburn stage,suggesting that gastricmucosal ischemia and hypoxia with resultantdisturbance in energy metabolism,but notgastric acid proper,might be the decisive factorin the pathogenesis of AGML after thermalinjury,and that the preventive use of anti-aciddrugs during burn shock period wasunreasonable in some respects.Therefore,taking effective measures to improve gastricmucosal blood perfusion as early as possiblepostburn might be more preferable for the AGMLprevention and treatment.

No relationship between IL-1B gene polymorphism and gastric acid secretion in younger healthy volunteers

AIM: To investigate the influence of IL-1B-511 gene polymorphism on IL-1B mRNA expression and gastric acid output in individual with or without Helicobacter pylori (H pylori) infection.METHODS: IL-1B mRNA expression and gastric acid secretion in 117 health volunteers were assayed using semi-quantitative RT-PCR and gastric juice assay, respectively. Pepsinogen (PG) Ⅰ and Ⅱ of 255 subjects (including 117 health volunteers) were also examined.RESULTS: T/T genotype individuals with H pylori infection had a more decreased PG Ⅰ/Ⅱ ratio. In gastric antrum mucosa, the individuals with H pylori infection had higher IL-1B expression than those without H pylori infection, but there was no obvious difference among each genotype. In gastric corpus, the individuals with H pylori infection had a significantly higher IL-1B expression than those without H pylori infection. IL-1B-511T/T genotype was markedly higher as compared with the other two genotypes. Both maximal acid output and basic acid output were similar among each genotype in IL-1B-511 gene locus, regardless of H pylori infection.CONCLUSION: IL-1B-511 T allele does not decrease gastric acid output, although it has a stimulated influence on IL-1B expression. Consequently, the pathway,through which IL-1B plays a central role in gastric cancer development, might not depend on low acid, but on the other regulation mechanisms.

Effects of nuclei ambiguus and dorsal motor nuclei of vagus on gastric H^+ and HCO_3^- secretion in rats

AIM: To determine the effects of electrical stimulation of nucleus ambiguus (NA) and dorsal motor nuclei of vagus (DMV) on gastric acid and bicarbonate secretion in rats. METHODS: NA and DMV in rats were electrically stimulated. Pylorus ligation or esophagus perfusion was used to collect the gastric secretion. The titratable H+ quantum, H+ concentration, HCO3- secretion quantum were measured. RESULTS: Electrical stimulation of NA had no effects on the volume of gastric juice, titratable acidity and acid concentration, but elicited a pronounced increase in the total bicarbonate. However, electrical stimulation of DMV significantly increased the titratable acidity, the volume of gastric juice and the acid concentration. Similarly, electrical stimulation of either NA or DMV decreased the respiratory frequency and sinus bradycardia. CONCLUSION: NA in rats can not control the secretion of gastric acid but the secretion of bicarbonate in gastric juice, while DMV controls the secretion of gastric acid.

Lead exposure increases oxidative stress in the gastric mucosa of HCl/ethanol-exposed rats

AIM: To investigate the role of reactive oxygen species in the ulcer-aggravating effect of lead in albino rats. METHODS: Albino Wistar rats were randomly divided into three groups and treated orally with 100 mg/L (low dose) or 5000 mg/L (high dose) of lead acetate for 15 wk. A third group received saline and served as control. At the end of wk 15, colorimetric assays were applied to determine the concentrations of total protein and nitrite, the activities of the oxidative enzymes catalase and superoxide dismutase, and lipid peroxidation in homogenized gastric mucosal samples. RESULTS: Exposure of rats to lead significantly increased the gastric mucosal damage caused by acidified ethanol. Although the basal gastric acid secretory rate was not significantly altered, the maximal response of the stomach to histamine was significantly higher in the lead-exposed animals than in the unexposed control group. Exposure to low and high levels of lead significantly increased gastric lipid peroxidation to 183.2% ± 12.7% and 226.1% ± 6.8% of control values respectively (P < 0.0). On the other hand, lead exposure significantly decreased catalase and superoxide dismutase (SOD) activities and the amount of nitrite in gastric mucosal samples. CONCLUSION: Lead increases the formation of gastric ulcers by interfering with the oxidative metabolism in the stomach.

Direct measurement of gastric H^+/K^+-ATPase activities in patients with or without Helicobacter pylori-associated chronic gastritis

AIM:The role of Helicobacter pylori (H pylori) infection in gastric acid secretion of patients with chronic gastritis remains controversial. This study was designed to elucidate the effect of H pylori on H+/K+-ATPase activities in gastric biopsy specimens. METHODS: Eighty-two patients with chronic gastritis who had undergone upper endoscopy were included in this study. H pylori infection was confirmed by rapid urease test and histology. Gastric H+/K+-ATPase activities and serum gastrin concentrations were measured by an enzymatic method and radioimmunoassay, respectively. For those patients who received triple therapy for eradicating H pylori, changes in the activity of gastric H+/K+-ATPase and serum gastrin levels were also measured. RESULTS: The mean gastric H+/K+-ATPase activity in Hpylori-positive group (42 patients) was slightly higher than that in Hpylori-negative group (29 patients) (169.65±52.9 and 161.38±43.85nmol P/(mg·h),respectively, P=0.301). After eradication of H pylori, the gastric H+/K+-ATPase activities slightly decreased compared to prior therapy (165.03±59.50 and 158.42±38.93 nmol P/(mg·h), respectively, P=0.805). The mean basal gastrin concentration was slightly higher in H pylori-positive patients than in H pylori-negative patients (87.92±39.65 pg/mL vs75.04±42.57 pg/mL, P= 0.228). The gastrin levels fell significantly after the eradication of H pylori. (Before treatment 87.00±30.78 pg/mL, after treatment 64.73±18.96 pg/mL, P=0.015). CONCLUSION: Gastric H+/K+-ATPase activities are not associated with H pylori status in patients with chronic gastritis.

Effect of somatostatin analogue octreotide injected into the third cerebral ventricle on pentagastrin-induced gastric acid secretion in rats

AIM： To investigate the effect of long-lasting somatostatin analogue octreotide （Oct） injected into the third cerebral ventricle （TCV） on gastric acid secretion in rats. METHODS： TCVs were cannulated in male Wistar rats anesthetized with sodium pentobarbital. One week later acute gastric lumen perfusion was carried out and gastric acid was continuously washed with 37℃ saline by a perfusion pump. Gastric perfusion samples were collected every 10 min and titrated by 0.01 moL/L NaOH to neutral. On the basis of subcutaneous （sc） injection of pentagastrin （G-5, 160 μg/kg）, Oct （0.025 μg, 0.05 μg, 0.1 μg, n=12 in each group） or vehicle （pyrogen-free physiological saline, n = 10） was injected into the TCV, Before and after the TCV injection, 1 h total acid output （TAO） was determined and experimental data were expressed in change rate （%） of TAO. RESULTS： Oct （0.025, 0.05 and 0.1 μg） injected into the TCV resulted in change rate of 1.56% （P〉0.05）, 20.21% （P〈 0.01） and 37.82% of TAO （P〈 0.001）, respectively. Moreover, comparison in change rate of TAO among these 3 doses showed P〈 0.05 between 0.025μg and 0.05 μg, P〈 0.01 between 0.025 μg and 0.ling, and P〈 0.05 between 0.05μg and 0.1 μg. However, sc injection of 0.05 μg Oct had no effect on G-5 stimulated gastric acid secretion. CONCLUSION： Octreotide injected into the third cerebral ventricle inhibits gastrin-induced gastric acid secretion in a dose-dependent manner.

Gastric acid level of humans must decrease in the future

Proton pump inhibitors strongly inhibit gastric acid production,but digestion problems do not generally arise.We can intake almost ordinary food even after total gastrectomy.Small intestine itself can digest and absorb food using various digestive enzymes without digestion in the stomach.The pH level of gastric acid in humans is much lower than that of most animals,and very close to that of carrion-eating animals called scavengers.It is assumed that ancient humans became bipedal approximately 4 million years ago.It was difficult for humans,who just started unstable bipedal locomotion,to catch quadrupedal-walking animals that can move faster,without special hunting tools.They may have eaten remaining carcasses,which is mainly the leftovers of carnivora species,as animalderived food.The benefit to produce a volume of gastric acid for humans is carrion eating,in which disinfection by gastric acid is important.Humans produce a high concentration of gastric acid to enable consumption of a diet containing some bacteria and support this lifestyle by consuming significant energy to protect themselves from gastric acid.Now,the opportunity for strong deleterious bacteria to enter the gastrointestinal tract has decreased because of the organized clean environment.If this hygienic environment is maintained for a long time,our gastric acid level must be decreased gradually.

Influence of gastric inhibitory polypeptide on pentagastrinstimulated gastric acid secretion in patients with type 2 diabetes and healthy controls

AIM： Gastric inhibitory polypeptide is secreted from intestinal K-cells in response to nutrient ingestion and acts as an incretin hormone in human physiology. While animal experiments suggested a role for GIP as an inhibitor of gastric secretion, the GIP effects on gastric acid output in humans are still controversial. METHODS： Pentagastrin was administered at an infusion rate of 1 μg . kg^-1 . h^-1 over 300 min in 8 patients with type 2 diabetes （2 female, 6 male, 54± 10 years, BMI 30.5 ± 2.2 kg/m^2; no history of autonomic neuropathy） and 8 healthy subjects （2/6, 46 ± 6 years., 28.9 ± 5.3 kg/ m^2）. A hyperglycaemic clamp （140 mg/dl） was performed over 240 min. Placebo, GIP at a physiological dose （1 pmol . kg^-1 . min^-1）, and GIP at a pharmacological dose （4 mol . kg^-1 . min^-1） were administered over 60 min each. Boluses of placebo, 20 pmol GIP/kg, and 80 pmol GIP/kg were injected intravenously at the beginning of each infusion period, respectively. Gastric volume, acid and chloride output were analysed in 15-min intervals. Capillary and venous blood samples were drawn for the determination of glucose and total GIP. Statistics were carried out by repeated-measures ANOVA and one-way ANOVA. RESULTS： Plasma glucose concentrations during the hyperglycaemic clamp experiments were not different between patients with type 2 diabetes and controls. Steady-state GIP plasma levels were 61 ±8 and 79 ± 12 pmol/I during the low-dose and 327±35 and 327± 17 pmol/I during the high-dose infusion of GIP, in healthy control subjects and in patients with type 2 diabetes, respectively （P= 0.23 and p 0.99）. Pentagastrin markedly increased gastric acid and chloride secretion （P〈 0.001）. There were no significant differences in the rates of gastric acid or chloride output between the experimental periods with placebo or any dose of GIP. The temporal patterns of gastric acid and chloride secretion were similar in patients with type 2 diabetes and healthy controls （P= 0.86 and P= 0.61, respectively）. CONCLUSION： Pentagastrin-stimulated gastric acid secretion is similar in patients with type 2 diabetes and healthy controls. GIP administration does not influence gastric acid secretion at physiological or pharmacological plasma levels. Therefore, GIP appears to act as an incretin rather than as an enterogastrone in human physiology.

Bravo capsule system optimizes intragastric pH monitoring over prolonged time:Effects of ghrelin on gastric acid and hormone secretion in the rat

AIM: To evaluate measurements of intragastric pH with the Bravo capsule system over a prolonged time.METHODS: A Bravo capsule was placed inside the rat gastric body and pH was studied for periods up to five consecutive days.For comparison,a gastric fistula model was used.Effects of ghrelin and esomeprazole,with or without pentagastrin,on gastric pH were studied.In addition,effects of esomeprazole on plasma ghrelin,gastrin and somatostatin were analyzed.RESULTS: All rats recovered after surgery.The average 24-h pH during free feeding was 2.3 ± 0.1 (n = 20) with a variation of 18% ± 6% over 5 d.Ghrelin,2400 pmol/kg,t.i.d.increased pH from 1.7 ± 0.1 to 3.1 ± 0.3 (P < 0.01) as recorded with the Bravo system.After esomeprazole (1 mg/kg,3 mg/kg and 5 mg/kg) there was a dose-dependent pH increase of maximally 3.4 ± 0.1,with day-to-day variation over the entire period of 8% ± 3%.The fistula and pH studies generated similar results.Acid inhibition with esomeprazole increased plasma ghrelin from 10 ± 2 pmol/L to 65 ± 26 pmol/L (P < 0.001),and somatostatin from 10 ± 2 pmol/L to 67 ± 18 pmol/L (P < 0.001).CONCLUSION: pH measurements with the Bravo capsule are reliable,and comparable to those of the gastric fistula model.The Bravo system optimizes accurate intragastric pH monitoring over prolonged periods and allows both short-and long-term evaluation of effects of drugs and hormones.

Physiological and clinical significance of enterochromaffin-like cell activation in the regulation of gastric acid secretion

Gastric acid plays an important role in digesting food （especially protein）, iron absorption, and destroying swallowed micro-organisms. H＋ is secreted by the oxyntic parietal cells and its secretion is regulated by endocrine, neurocrine and paracrine mechanisms. Gastrin released from the antral G cell is the principal physiological stimulus of gastric acid secretion. Activation of the enterochromaffin-like （ECL） cell is accepted as the main source of histamine participating in the regulation of acid secretion and is functionally and trophically controlled by gastrin, which is mediated by gastrin/CCK-2 receptors expressed on the ECL cell. However, longterm hypergastrinemia will induce ECL cell hyperplasia and probably carcinoids. Clinically, potent inhibitors of acid secretion have been prescribed widely to patients with acid-related disorders. Long-term potent acid inhibition evokes a marked increase in plasma gastdn levels, leading to enlargement of oxyntic mucosa with ECL cell hyperplasia. Accordingly, the induction of ECL cell hyperplasia and carcinoids remains a topic of considerable concern, especially in long-term use. In addition, the activation of ECL cells also induces another clinical concem, i.e., rebound acid hypersecretion after acid inhibition. Recent experimental and clinical findings indicate that the activation of ECL cells plays a critical role both physiologically and dinically in the regulation of gastric acid secretion.

Effects of Supplemental Histamine on Gastric Acid Secretion, Digestive Enzyme Activities, Intestinal Microfloral of Early Weaned Piglets

Two experiments were conducted to study the effect of supplemental histamine in the diet of early-weaned piglets. In experiment A, 24 cross bred piglets with an average body weight of 6.10±0. 40 kg, weaned at the age of 28 days, were divided into four groups, fed with basal diet of low dietary copper without (control) or with supplemental histamine at 60, 120, 180μg kg-1 BW. During the two weeks and the third week after weaning, ADG(average daily gain) of piglets were increased by 15.8%(P<0. 05), 9.5%(P< 0.10) by addition of 60μg kg-1 BW histamine, but decreased by addition of 180μg kg-1BW histamine, which also increased the amount of E. coli in colon and the scour incidence. The secretion of gastric acid and pepsin were improved by both dose of supplemental histamine (60, 180μg kg-1BW) and gastric digesta pH were decreased by both. Addition of 60 μg kg-1 BW histamine improved the activities of trypsin, amylase in duodelum digesta. In experiment B, 12 cross bred piglets with an average body weight of 6. 85±0.35 kg, weaned at the age of 28 days, were divided into two groups, fed with basal diet of high dietary copper without (control) or with supplemental 60 μg kg-1 BW histamine. During the two weeks and the third week after weaning, ADG of piglets were increased by 9. 8% (P<0.05), 7. 0% (P<0. 10). The secretion of gastric acid, activities of trypsin and amylase in duodelum digesta, were also improved by addition of 60 μg kg-1BW histamine. The results showed that addition of histamine (60μg kg-1BW) in early weaned piglets could increase the secretion of gastric acid and pepsin, reduce gastric digesta pH and scour incidence, improve activities of trypsin, amylase in duodelum digesta, and the growing performance of early weaned piglets.

Gastric Mucosal Blood Flow and Acid Secretion in Rats

The relationship between gastric mucosal blood flow (GMBF) and gastric acid secretionwere studied in rats by using secretory stimulant (pentagastrin)and inhibitor(cimetidine). GMBFwas measured by Laser Doppler flowmetry (LDF) and gastric mucosal pH determined by microglasspH electrode. GMBF increased and gastric mucosal pH decreased significantly after intravenous injec-tion of 6μg/kg of pentagastrin; nevertheless GMBF decreased and gastric mucosal pH increasedmarkedly after intravenous administration of 100mg/kg of cimetidine. This indicates that pentagastrincan increase GMBF and gastric acid secretion, and cimetidine can decrease GMBF and gastric acidsecretion in rats, proving the close relationship between GMBF and gastric acid secretion in rats.

Construction and Expression of Recombinant Ghrelin Plasmid and Effects on Growth Performance and Gastric Acid Secretion of Rats

The paper was to study construction and expression of rGhrelin （pcDNA3 -Ghrelin） and its effect on growth performance and gastric acid secretion of rats. Ghrelin amplified from gastric mucosa of weaned piglets was cloned into the expression vector pcDNA3 to get recombinant plasmid pcDNA3 - Ghrelin. Twelve weaning rats were randomly divided into two groups, six rats each group. The rats in each treatment group were individually injected with 100pg of naked plasmid pcDNA3 -Ghrelin, and the rats in control group were injected with empty plasmid. The weights and feed consumption of rats were measured after injection for 7, 14 and 29 d, respectively. The rats were sacrificed at the end of the experiment, and their stomach was separated and weighed, the pH value of gastric juice was measured as well. The results showed that the average daily gain of rats at 7 and 29 d were significantly higher than that in control group, respectively （P〈0.05）, and feed consumption did not have significant chan- ges; the feed meat ratio of rats in the treatment groups was significantly lower than that in control group （ P 〈0.05） ; the gastric relative weight and gastric weight did not change significantly, while the pH value of gastric juice of rats in treatment groups was significantly lower than that in control group （P 〈 0.05）. This indicated that after transfected expression of muscle tissue, ghrelin played an important regulatory role in growth and gastric acid secretion of rats.

Two-Dimensional pH Mapping of a Histamine-Stimulated Gastric Mucosa by Using an Ion Image Sensor in the Guinea Pig

In order to examine the hydronium ion （proton）-releasing functions in cells, [pH]out （extracellular pH） was measured using an ion image sensor composed of a 2D （two-dimensional） array of potential sensitive pixels. Using gastric tissues prepared from the stomach, pH distribution was observed during the histamine stimulation. The 2D distribution of [pH]out in the gastric tissues showed clear differences between the mucosal sides and the serous side. Even before the histamine stimulation, the mucosal side of the gastric mucosa showed a slightly lower pH than that of serous side. In the mucosal side, [pH]out decreased after the onset of the stimulation. The ion image sensor was capable of visualizing [pH]out in the gastric tissues. The present chemical-sensing technique realized a label-free microscopic assessment of the 2D distributions of biologically interesting substances, and consequently, [pH] out imaging via chemical microscopy has a future potential in medical fields for endoscopic analysis of gastric ulcers.

Diagnostic value associated with the combination of saliva pepsin and microorganisms in functional heartburn and gastroesophageal reflux disease

Heartburn is a common symptom shared by both gastroesophageal reflux disease(GERD)and functional heartburn(FHB),which can make it challenging to differentiate between the two conditions.However,examining oral manifestations of GERD can be a cost-effective and readily available method to aid in this differentiation process.It may serve as a valuable tool in distinguishing GERD from FHB.

Brain-gut axis in the pathogenesis of Helicobacter pylori infection

Helicobacter pylori (H. pylori) infection is the main pathogenic factor for upper digestive tract organic diseases. In addition to direct cytotoxic and proinflammatory effects, H. pylori infection may also induce abnormalities indirectly by affecting the brain-gut axis, similar to other microorganisms present in the alimentary tract. The brain-gut axis integrates the central, peripheral, enteric and autonomic nervous systems, as well as the endocrine and immunological systems, with gastrointestinal functions and environmental stimuli, including gastric and intestinal microbiota. The bidirectional relationship between H. pylori infection and the brain-gut axis influences both the contagion process and the host&#x02019;s neuroendocrine-immunological reaction to it, resulting in alterations in cognitive functions, food intake and appetite, immunological response, and modification of symptom sensitivity thresholds. Furthermore, disturbances in the upper and lower digestive tract permeability, motility and secretion can occur, mainly as a form of irritable bowel syndrome. Many of these abnormalities disappear following H. pylori eradication. H. pylori may have direct neurotoxic effects that lead to alteration of the brain-gut axis through the activation of neurogenic inflammatory processes, or by microelement deficiency secondary to functional and morphological changes in the digestive tract. In digestive tissue, H. pylori can alter signaling in the brain-gut axis by mast cells, the main brain-gut axis effector, as H. pylori infection is associated with decreased mast cell infiltration in the digestive tract. Nevertheless, unequivocal data concerning the direct and immediate effect of H. pylori infection on the brain-gut axis are still lacking. Therefore, further studies evaluating the clinical importance of these host-bacteria interactions will improve our understanding of H. pylori infection pathophysiology and suggest new therapeutic approaches.

Influence of H pylori on plasma ghrelin in patients without atrophic gastritis

AIM:To determine the association between H pylori infection and serum ghrelin levels in patients without atrophic gastritis.METHODS:Fifty consecutive patients(24 males and 26 females)with either H pylori-positive gastritis(n = 34)or H pylori-negative gastritis(n = 16)with normal gastric acid secretion determined by 24-h pHmetry and without atrophic gastritis in histopathology were enrolled in this study.Thirty-four H pylori-infected patients were treated with triple therapy consisting of a daily regimen of 30 mg lansoprazole bid,1 g amoxicillin bid and 500 mg clarithromycin bid for 14 d,followed by an additional 4 wk of 30 mg lansoprazol treatment.H pylori infection was eradicated in 23 of 34(67.6%)patients.H pylori-positive patients were given eradication therapy.Gastric acidity was determined via intragastric pH catethers.Serum ghrelin was measured by radioimmunoassay(RIA).RESULTS:There was no signifficant difference in plasma ghrelin levels between H pylori-positive and H pylori-negative groups(81.10 ± 162.66 ng/L vs 76.51 ± 122.94 ng/L).In addition,there was no significant difference in plasma ghrelin levels and gastric acidity levels measured before and 3 mo after the eradication therapy.CONCLUSION:H pylori infection does not influence ghrelin secretion in patients with chronic gastritis without atrophic gastritis.

Effect of Lanthanum on Acid Secretion from Isolated Mouse Stomach in Vitro

To explore the effect and the mechanism of La^(3+) on gastric acid secretion (GAS) of isolated mouse stomach with perfused lumen, 12 cm H_2O column intragastric pressure-provided, whole stomach preparations from mice were incubated in buffer at 37 ℃ in vitro, and perfusate was measured for pH with a pHS-3 type pH meter. The results show that La^(3+) (0.41～820×10^(-6) mol·L^(-1)) significantly promotes GAS in a concentration-dependant manner. Proglutamine, a blocker of gastrin receptor, potently inhibits GAS, and it may block the promotive effect of La^(3+) on GAS, and this effect increases with the increase of proglutamin concentration. Cimetidine, a blocker of histamine H_2 receptor, also potently inhibits GAS, and blocks the promotive effect of La^(3+) on GAS in the same manner with proglutamine. These results suggest that La^(3+) promotes GAS in isolated stomach possibly by stimulating the releases of gastrin from G cell and Histamine from ECL cell or by activating the gastrin receptors and Histamine H_2 receptors on the parietal cell, thereby accelerating the acid secretion of parietal cells in stomach.