Cirugía de supresión ácida y derivación duodenal laparoscópica vs abierta en esófago de Barrett extenso: resultados y complicaciones a corto y largo plazo / Laparoscopic versus open fundoplication with acid suppression/duodenal diversion technique for long segment Barrettís esophagus

Resumen Introducción: En pacientes con esófago de Barrett largo hemos sugerido efectuar fundoplicatura con antrectomía, vagotomía y derivación duodenal en Y de Roux que podría asociarse con complicaciones y efectos colaterales. Objetivo: El objetivo de este estudio es comparar la cirugía por vía abierta vs laparoscópica en cuanto a complicaciones postoperatorias precoces y alejadas, mortalidad y resultados alejados. Material y método: Se comparan 2 cohortes de pacientes, 73 pacientes con cirugía abierta y 53 pacientes operados con la misma técnica por vía laparoscópica por el mismo equipo. Solo se incluyeron los pacientes con Barret largo. Se controlan clínicamente en el postoperatorio inmediato y alejado, con endoscopia e histología anual, y se evalúan los resultados en cuanto a complicaciones precoces, alejadas y se analiza la calidad de vida y la satisfacción del paciente. Para el análisis se utilizó «t¼ de Student considerando un valor de p < 0,05 como significativo. Resultados: En cuanto a complicaciones precoces en ambos grupos no hubo diferencias significativas. No hubo mortalidad postoperatoria. En las complicaciones tardías las complicaciones totales no son significativamente diferentes entre ambos grupos (solo cambian sus causas y características) ni en cuanto a la clasificación de Visick y el puntaje de calidad de vida. Conclusión: La fundoplicatura con procedimiento de supresión ácida y derivación biliar por vía laparoscópica presenta similares resultados a corto y largo plazo que la cirugía abierta, pero con los beneficios de una cirugía mínimamente invasiva.

Abstract Introduction: In patients with long Barrett esophagus we have suggested to perform fundoplication with antrectomy, vagotomy and Roux-en-Y duodenal diversion however it could be associated with complications and side effects. Objective: The objective of this study is to compare open versus laparoscopic surgery for early and early postoperative complications, mortality and distant outcomes. Material and method: We compare 2 cohorts of patients, 73 patients with open surgery and 53 patients, who underwent laparoscopic surgery using the same technique. Only patients with Long Barrett were included. They are clinically monitored in the early and late postoperative period, with endoscopy and histology at long term follow-up (3-5 years). The results were evaluated in terms of early and late complications, the quality of life and patient satisfaction were analyzed. For the analysis we used t-student considering a P < .05 as significant. Results: As for early complications, there were no significant differences in both groups. There was no postoperative mortality. In the late complications, the total complications are not significantly different between the two groups (only their causes and characteristics changed) neither in terms of Visick's classification and the quality of life score Conclusion: The fundoplication, with laparoscopic acid suppression and duodenal diversion, presents similar short-term and long-term results than open surgery, with the benefits of a mini-invasive procedure.

Effect of Zinc Salts on Acid Secretion and Peptic Ulceration in Albino Rats.

The present study was carried out to see the effect of two zinc salts i.e zinc sulphate and zinc chloride on gastric ulcers induced by stress, pylorus ligation and aspirin in albino rats. The rats were divided into two main groups (zinc sulphate 30, 60, 90 mg/kg i.p and zinc chloride 10 and 20mg/kg i.p). They were further sub-divided into three sub-groups dependant on ulcer model i.e stress, pylorus ligation and aspirin induced ulcers. It was found that zinc sulphate and zinc chloride had a dose dependant reduction in ulcer index in all three models of gastric ulceration. Also, both the salts had anti acid secretory effect, raised pH of gastric secretion and reduced total acidity significantly. Thus zinc salts prevent gastric ulceration. Probably this effect is mediated by anti acid secretory action.

Evaluating ranitidine, pantoprazole and placebo on gastric pH in elective surgery

Concern about the grim nature of postoperative acid aspiration syndrome grew among the anesthesiologist over the years warranting the need for preemptive intervention. The aim of the study is to compare the effects of preoperative oral ranitidlne versus pantoprazole given in regulating gastric pH in elective surgery. This prospective, parallel group, controlled, randomized, single-blind study was conducted at a tertiary care postgraduate teaching institute at Kolkata, involving 120 participants of either sex, aged 18-60 years of American Society of Anesthesiologists physical status I and II, who were scheduled for elective surgery under general anesthesia lasting for more than 2 h. The participants were divided into three groups. In group A [n = 40] participants received placebo tablet, in group B [n = 40] participants received ranitidine tablet while in group C [n = 40], participants received pantoprazole tablet and their gastric pH estimated serially. The participants in the three groups were comparable in terms of age, sex, body weight, duration of surgery and type of surgery distribution. In regard to changes in gastric pH trends, there was no statistically significant difference between serial pH values in group A [Friedman test; P>0.05] and group C participants. [P>0.05]. However, the mean preoperative gastric pH values [7.140 +/- .7652] were significantly lower than mean pH values [7.253 +/- .7514] after 2 h postoperatively in group B participants [P<0.05]. From the observations and analyses of the present study, it can be inferred that ranitidine is more effective than pantoprazole to raise the gastric pH for prevention of aspiration pneumonitis

Lead exposure changes gastric acid secretion in rat: role of nitric oxide [No]

Sub chronic exposure to lead in rats slows gastric emptying, but little is known about the effects of lead on gastric secretion. This study was designed to investigate the effects of lead on gastric acid secretion and its possible mechanisms in rats. Lead acetate was dissolved in drinking water in a concentration of 1%. Sodium acetate-containing water with a molar concentration similar to lead was also prepared. We had nine groups of animals [n=8]; four of them were exposed to lead for 1, 2, 3, and 4 weeks [Pbl, Pb2, Pb3 and Pb4 groups, respectively]. Sodium acetate solution was given to another four groups for 1, 2, 3, and 4 weeks [Nal, Na2, Na3 and Na4 groups, respectively]. Gastric secretion was collected by washout technique and its acid output was measured in the basal [Basal Acid Output, BAO], vogotomy [Vagotomized Acid Output, VAO], and vagally stimulated [Vagally Stimulated Acid Output, VSAO] states using titrator instrument. Nitric oxide [NO] metabolite of gastric tissue was determined by Griess micro assay method to evaluate the possible mechanism of lead effect on gastric secretion. VSAO was significantly less in Pbl and Pb2 groups than Nal and Na2 ones respectively [1.75 +/- 0.17, 2.10 +/- 0.30 vs. 5.79 +/- 0.20, 6.18 +/- 0.27 micromol/15min] [P=0.001, P=0.001] BAO was significantly more in Pb3 and Pb4 groups than Na3 and Na4 ones respectively [2.77 +/- 0.37, 2.80 +/- 0.31 vs. 1.73 +/- 0.16, 1.79 +/- 0.34 micromol/15min] [P=0.01, P=0.02], but it was the same after vagotomy. VSAO was more in Pb3 and Pb4 groups than their Na counterparts [P=0.001, P=0.0001] NO metabolite of gastric tissue was more in all Pb groups in comparison to their Na counterparts [P=0.0001]. In this study, it seems that lead exposure, via NO mechanism, has different effects on acid secretion. Nitric oxide in small and large amounts decrease and increase gastric acid secretion, respectively

Effect of oral [systemic] Elaeagnus angustifolia L. Fruit on stimulated gastric acid secretion in unconscious rat and on basal acid secretion in conscious rat

It has been clearly documented that Elaeagnus angustifolia [E.A.] have variety of medicinal uses including anti - ulcerogenic activity. Our recent study demonstrates that intragastric administration of E.A. blocked the carbachol - induced gastric acid secretion, completely. The aim of this work therefore is to evaluate the role of oral administration of E.A. on carbachol - induced gastric acid secretion in order to compare with intragastric effect of the drug. We also hypothesized that E.A. fruit might be involved in control of basal acid secretion and juice volume. To address this question, we investigated the oral effect of E.A. fruit extract on basal acid secretion on pylorous - ligated conscious rats. In this study we used pylorus ligation method. Briefly, animals were anesthetized and two cannulas were introduced into the stomach through esophagus to wash the stomach and pylorousdodenal junction to collect the stomach juice. Carbachol was infused into jugular vein and gastric juice was collected in 10 - min periods to titrate with NaOH 0.01 N. To concider the effect of the E.A. extraction on basal acid secretion, all experiments were performed in conscious rats who received the E.A. extract or saline 1.5 hours before pylorus-ligation. Ligation of pylorus was performed under brief ether anesthetized. Two and half hours after treatment, the stomach was removed, juice volume was measured and acid output was determined as above. Statistical analysis was performed by analysis of variance and subsequent tukey test. Our results showed that the E.A. fruit extract dose dependently decreased the carbachol - induced gastric acid secretion. Stimulated acid secretion was suppressed%52 +/- 4 at a dose 600 mg/kg and this inhibitory effect persisted up to the end of experiments.Oral administration of E.A. extraction in pylorus ligated conscious rats showed that the drug significantly stimulated gastric acid secretion and juice volume at a dose 1300 mg/kg within 1 hour, but there was no effect at lower doses. These results suggest that E.A. fruit has an anti-secretory action on cholinergic stimulated acid secretion by oral administration. This effect is less than the intragastric administration of the drug [% 81 +/- 4 inhibition]. It is likely that the inhibitory effect is mediated by cholinergic nervous system and/or non-neuronal membranes. We also suggest that the oral E.A. extract has no effect on basal acid secretion at lower doses

Gastrointestinal bleeding in a toddler secondary to chronic renal failure and hyper-gastrinemia.

A 3-year-old girl with H. pylori negative duodenal ulcer with hypergastrinemia secondary to chronic renal failure presenting with upper gastrointestinal bleed as the cardinal manifestation is unusual in toddlers and the case is presented for its rarity.

[Intragastric effect of Elaeagnus angustifolia L. fruit on gastric acid secretion in a rat pylorus - ligated model]

It has been clearly documented that Elaegnaceae have a variety of medicinal uses including anti-ulcerogenic activity. We therefore hypothesized that Elaeagnus angustifulia L. [E. A.] fruit might be involved in the control of stimulated gastric acid secretion. To address this question, we investigated the pharmacological effect of the E. A. fruit extract on carbachol-induced acid secretion in a pylorus-ligated rat. In this study we used pylorus ligation method. Briefly, animals were anesthetized and two cannulas were introduced into the stomach through esophagus to inject drug and pylorododenal junction to collect the stomach juice. Carbachol or histamine was infused into jugular vein and gastric juice was collected in 10-min periods to titrate with NaOH 0.01 N. Our results showed that the E. A. fruit extract dose and time dependently decreased the carbachol- [but not histamine-] stimulated gastric acid secretion when it administered at increased steady level [at 30 minute] of carbachole time-course curve. Stimulated acid secretion was completely suppressed at a dose 600 mg/kg 30 min after drug administration and this inhibitory effect persisted up to the end of experiments [100 min]. Using E.A. fruit extract simultaneously with carbachol infusion had no effect on acid secretion. These results suggested that E.A. fruit has a pH-dependent anti-secretory action on cholinergic-stimulated gastric acid secretion by intragastric administration. It is likely that the inhibitory effect is mediated by cholinergic nervous system and/or non-neuronal membranes

[ effect of baclofen on treatment of infancy gastro-esophageal reflux disorder]

Transient lower esophageal sphincter relaxation [TLESR] is the major cause of gastro-esophageal reflux disorder [GERD] in patient with reflux disease. GERD is the most common esophageal disorder in children. The GABA agonist baclofen decreases acid reflux through the inhibition of TLESRs and should similarly decrease non-acid reflux. The aim of this study was to evaluate the effect of baclofen on GERD in children. Thirty children with GERD were included in this clinical trial. Baclofen 0.25 mg/kg was given for three months. End points were assessed for weeks and months. Baclofen significantly improved the weight gain pattern and the mean of weight gain demonstrated a significant difference between base line value and weight on consequent months after therapy [P<0.0001]. Restlessness showed a significant improvement between baseline and threes month after treatment [P<0.001].Vomiting significantly decreased on follow up visits [P<0.001]. It is also increased the time and volume of feeding significantly 3 month after treatment [P<0.001]. We have not found serious complications. Baclofen reduces the symptom of TLESRs and may have a role in treating GERD

The Role of Gastric Acid in the H. pylori-induced Gastritis in Mouse / 대한소화기학회지

BACKGROUND/AIMS: This study was designed to investigate the role of gastric acid in the extent of H. pylori-induced gastritis. METHODS: Twenty eight mice were innoculated with live H. pylori. They were allocated into four groups. Mice in group I received no treatment, group II mice were treated with sham injection, group III received 125microgram/kg body weight of pentagastrin, while group IV received 250microgram/kg body weight of pentagastrin subcutaneously three times a week. After 7 months, the mucosal pH, H. pylori density, neutrophils and monocytes infiltration, and the degree of atrophy were assessed in the stomach. RESULTS: In the gastric body, the densities of H. pylori were not different among groups. The degree of neutrophil infiltration was significantly lower in group IV compared to other groups (p<0.05). The degree of monocyte infiltration was also significantly lower in group IV than group III (p<0.05). In the gastric antrum, there was no significant difference of the H. pylori density, neutrophil and monocyte infiltration, and degree of atrophy among the groups. The mice with the gastric mucosal pH lower than mean of 3.2 had significant lower level of H. pylori density (1.4 vs. 2.4, p=0.04), and infiltration of neutrophils (0.9 vs. 2.3, p=0.018), and monocytes (1.2 vs. 1.8; p=0.011) than the those with mucosal pH above 3.2 in the body of stomach. CONCLUSIONS: Gastric acid plays a role in suppressing the proximal propagation of H. pylori-induced gastritis to the body of stomach.

effect of Amirkabiria odoratissima extract on gastric acid and pepsin secretion level in rat

Amirkabiria odoratissima is widely used as an odorant in east south provinces. Many people believe that this plant is useful in treatment of some gastrointestinal disorders. Therefore, this study was conducted to investigate the effect of the plant extract on the secretion rate of acid and pepsin in the stomach of the rats studied. This is an experimental study involving 3 groups of rats, 8 in each group. The control group received placebo and case groups were received 100 mg/kg and 16.2 mg/kg of Amirkabiria odoratissima by gastrodeodenostomy canola. After anesthesia with nesdonal, 50 mg/kg IP, rats were gone under surgical process, tracheotomy. Subsequently, stomach secretion obtained using Wash Out method included in the first and the second base and measured acid by titrimetry method and pepsin by Anson method. Data were analyzed using t and ANOVA methods. The amount of acid significantly decreased in both Amirkabiria odoratissima groups compared to control group [p<0.001]. However, there was no significant change in pepsin secretion [p>0.05]. Using of Amirkabiria odoratissima decreases gastric acid secretion and may be useful in patients with gastro intestinal disorders

Effect of aqueous extract of neem (Azadirachta indica) leaves on offensive and diffensive gastric mucosal factors in rats.

Standardized aqueous extract of Neem (Azadirachta indica) leaves (AIE) has been reported to show both ulcer protective and ulcer healing effects in normal as well as in diabetic rats. To study the mechanism of its ulcer protective/healing actions, effects of AIE (500 mg/ kg) was studied on various parameters of offensive acid-pepsin secretion in 4 hr pylorus ligation, pentagastrin (PENTA, 5 microg/kg/hr)-stimulated acid secretion and gastric mucosal proton pump activity and defensive mucin secretion including life span of gastric mucosal cells in rats. AIE was found to inhibit acid-pepsin secretion in 4 hr pylorus ligated rats. Continuous infusion of PENTA significantly increased the acid secretion after 30 to 180 min or in the total 3 hr acid secretion in rat stomach perfusate while, AIE pretreatment significantly decreased them. AIE inhibited the rat gastric mucosal proton pump activity and the effect was comparable with that of omeprazole (OMZ). Further, AIE did not show any effect on mucin secretion though it enhanced life span of mucosal cells as evidenced by a decrease in cell shedding in the gastric juice. Thus, our present data suggest that the ulcer protective activity of AIE may be due to its anti-secretary and proton pump inhibitory activity rather than on defensive mucin secretion. Further, acute as well as sub acute toxicity studies have indicated no mortality with 2.5 g/kg dose of AIE in mice and no significant alterations in body or tissues weight, food and water intake, haematological profile and various liver and kidney function tests in rats when treated for 28 days with 1 g/kg dose of AIE.

[Effect of Heracleum persicum extract on acid and pepsin secretion level in both basic and stimulated conditions with pentagastrin in rat]

The Heraclleum persicum is widely used as an odorant in pickles around the world and particularly in Iran. As pickle is a gastric stimulator, the question is whether this plant which is used in making pickles, decreases gastric stimulation of this group of foods, or increases it, and in general, what is the cellular mechanism of this plant on acid and pepsin secretion. Therefore, in this study the effect of plant entrants on the secretion rate of acid and pepsin surveyed in the stomach in rats. This study involves two groups [12 in each group] of rats in experimental method [Control group and Heracleum group]. After anesthesia with nesdonal, 50 mg/kg IP, rats were gone under surgical process, tracheotomy, laparatomy and gasteroadeodenostomy and the Heraclleum extract [12.5 mg/kg] was send into the stomach from gasterodeodenostomy canula in Herculean group. The amount of both acid and pepsin in both basal and stimulated condition were significantly increased in heracleum group compared to control group [p<0.001]. Pentagastrin also increased acid and pepsin secretion in control group [p<0.001] and increased pepsin in heraclleum group [p<0.05] but did not significantly change in acid secretion in heraclleum group. The Heracleum persicum increases acid and pepsin secretion when is used in food regimen. Its extract also increases gastric acid secretion via blockage of gastric receptor. However, a different mechanism is involved in the increasing of pepsin secretion

effect of acute consumption of paraoxon on basal and Pentagastrin-Stimulated Gastric acid and pepsin secretion in rats

Paraoxon is an organophosphate. Organophosphate inhibit acetylcholinestrase enzyme and cause nicotinic and muscarinic sings. There is no study on our knowledge regarding the effect of these substances on gastric acid and pepsin secretion. In the present study, the effect of acute consumption of paraoxon on gastric acid and pepsin secretion has been investigated. In the present study 30 female N-mari rats weighing 200-250gr were used. The first group [paraoxon] received 0.5mg/kg paraoxon intraperitonealy. The second group [alcohol] received the dozes of ethyl alcohol [96%] and the third group [control] received no drug. Animals were anesthetized by intraperitoneal injection of 50mg/kg Sodium thiopental. After trachesotomy and laparatomy gastric secretions were collected with a tube via duodenum. Pentagastrin [25 micro g/kg. ip] was used as gastric stimulator. Acid and pepsin secretions were measured by titration and Anson methods respectively. Stages of measurement were basal, stimulated. and re-basal. The basal acid secretion in control, alcohol and paraoxon groups was 7.6 +/- 0.26, 7.46 +/- 0.4 and 7.03 +/- 0.28 micro mol/15min respectively that shows no significant difference among three groups. Although following pentagastrin-stimulation acid secretion was significantly more than basal stage in all groups, but there was significantly more secretion in control than alcohol subjects. But there was no difference between control and paraoxon or alcohol and paraoxon groups in this regard. Regarding pepsin secretion, there was significantly more secretion in alcohol subjects than others in all measured stages. In comparison to control group, acute paraoxon has no effect on basal acid pepsin secretion, while acute alcohol caused a significant increase in basal acid/pepsin secretion

Garlic effects on gastric acid and pepsin secretions in rat

Garlic [Allium Satiyum] is a plant widely used in traditional medicine. Its anti-hypertensive, lipid lowering, oxidative activities, anti-viral, anti-bacterial, anti-fungal properties have been proven. It has a tonic effects on stomach but its effects on gastric secretion is not known. To investigate the effect of garlic extract on basal and pentagastrin stimulated gastric acid and secretions in rats. Garlic extract stimulates gastric gland causing increased production/release of basal acid and pepsin level. Garlic acid mask pentagastrin stimulatory response and causes decrease in acid and pepsin secretary level. Two group of wistar rats [12 in each group] weighing 200-250gm were used. The first group was considered as study group and received garlic extract, the second group was considered as control. Animal were anesthetized with an intraperitoneal injection of sodium thiopental [50 mg/kg] and after tracheotomy and ligation of cervical esophagus, laparotomy was done. A cannula was placed in stomach through duodenum and 1ml of normal saline was injected in to stomach in each group. After 30 minutes their stomach were emptied. Next in study group 1ml garlic extract [100 mg/kg] and in control group 1ml normal saline were introduced into stomach. After 15 min 1ml normal saline was injected in both groups and immediately all gastric contents were collected in both groups by wash out technique and basal secretions of acid and pepsin were measured. In order to measure pentagastrin effect on gastric secretions, 25 micro gram/kg pentagastrin was used in both groups. Basal acid secretion in study group showed a significant increase in comparison to control group with P value <0.001 [15.6 +/- 1.63 micro mol/15 min in case group vs 4.1 +/- 0.36 micro mol/15min]. Basal pepsin secretion in study group showed a significant increase in comparison to control group with P value <0.001 [7.27 +/- 0.15 micro gm/15min in case group vs 5.62 +/- 0.12 micro gm/15min]. On pentagastrin stimulation, acid secretion in control group showed a significant increase in comparison to its basal value with P value <0.001 [10.14 +/- 1.34 micro mol/15min in vs 4.1 +/- 0.36 micro mol/15 min] but its value decreases in study group [10.5 +/- 1.89 micro mol/15min basal value]. In control group following pentagastrin stimulation, pepsin secretion showed a significant increase in comparison to its basal value with P value <0.001 [6.9 +/- 0.12 micro gm/15min in case group vs 5.62 +/- 0.12 micro gm/15min], while in study group there is no significant difference from its basal value [7.03 +/- 0.03 micro gm/15 min vs 7.27 +/- 0.15 micro gm/15 min basal value]. Garlic extract have a stimulatory effect on acid and pepsin secretion. The possible mechanism cloud be: a] Increase in parietal or chief cell activities due to Ach release. b] Due to its stimulatory effect on histamine release. However, on pentagastrin stimulation acid secretion decline and pepsin level remain same in study group and this effect may be due to rapid emptying of gastric acid stock or due to inhibition of gastric activity because of attachment of some components in garlic extracts to gastrin receptors on parietal cells

Mechanism of Actions and Clinical Applications of Proton Pump Inhibitors / 대한소화기학회지

Proton pump inhibitors (PPIs) are widely used in clinical practice from early 1990s for the treatment of acid- related diseases. PPIs are superior to histamine2-receptor antagonists or anticholinergic agents. These drugs have proven to be effective, safe and well-tolerated during the past two decades. This brief review presents the pharmacodynamics and pharmacokinetics of PPIs and presents clincal applications of the drugs in acid-related diseases.

effects of chronic consumption of heroin on basal and vagal electrical-stimulated gastric acid and pepsin secretion in rat

Addiction to opium and heroin is not only an important social and individual problem in the world but it also affects the human physiology and multiple systems. The aim of this study is to determine the effects of chronic heroin consumption on basal and vagus electrical-stimulated total gastric acid and pepsin secretion in rats. The study was carried out in the Department of Physiology, Kerman University of Medical Sciences, Iran from August 2002 to June 2003. Both male and female rats weighing 200-250g were used. Rats received daily doses of heroin intraperitoneally starting from 0.2 mg/kg to 0.1mg/kg/day up to the maintenance level of 0.7mg/kg and continued until day 12. After anesthesia, tracheotomy and laparotomy, gastric effluents were collected by washout technique with a 15 minutes interval. The total titrable acid was measured by manual titrator, and the total pepsin content was measured by Anson's method. Vagal electrical stimulation was used to stimulate the secretion of acid and pepsin. Heroin results in a significant decrease in total basal acid and pepsin secretions [4.10 +/- 0.18mmol/15 minutes versus 2.40 +/- 0.16mmol/15 minutes for acid, p<0.01, and 3.63 +/- 0.18 mg/15 minutes versus 3.11 +/- 0.18 mg/15 minutes for pepsin, p<0.05]. But, it does not produce any significant changes in acid and pepsin secretions in vagotomized condition. Heroin also causes a significant decrease in vagal-electrically stimulated acid and pepsin secretions [14.70 +/- 0.54 mmol/15 minutes versus 4.30 +/- 0.21mmol/15 minutes for acid, p<0.01, and 3.92 +/- 0.16 mg/15 minutes versus 3.37 +/- 0.16 mg/15 minutes for pepsin, p less than 0.05]. Heroin consumption decreases the total gastric basal and vagus stimulation of acid and pepsin secretion, but not in vagotomized condition. Heroin may decrease acid secretion by inhibiting vagal release of acetylcholine within the gastric wall. Other probable mechanisms include: presynaptic inhibition of acetylcholine release or depressing the vagal center, inhibition of pentagastrin induced acid secretion, inhibitory effects via central mechanisms, probably mediated by the opiate receptors. Further studies are needed to recognize the actual mechanism

Cigarette smoking and its effect on gastro-pharyngeal and gastro-esophageal refluxes

Ciastro-pharyageal reflux appears to be associated with various otolaryngological complaints Cigarette smoking is known to affect adversely the defense mechanisms against reflux of gastric acid into the esophagus. To study the relationship between gastropharyngeal as well as gastroesophageal refluxes and cigarette smoking, fifteen subjects underwent 24-hour double - probe pH monitoring while smoking their daily amount of cigarettes. The percentage of time the PH was below 4 during the smoking period was significantly higher than the percentage of time the pH was below 4 during the non-smoking period, proximal, at the level of the upper oesophageal sphincter, as well as distal above the lower oesophageal sphincter. in conclusion, this study demonstrated and concluded that smoking increases both the gastropharyngeal and gastroesophageal refluxes by affection on the defense mechanisms against reflux of gastric acid or increased gastric acidity. Thus, smokers with disorders and / or complaints caused by reflux should, therefore, be advised to stop smoking in order to reduce reflux of gastric acid into the oesophagus and pharynx

Evaluation of the gastric mucosal effects of different antidepressant drugs in the rat

Investigations were performed in the rat to evaluate the effects of different classes of antidepressant drugs on the gastric mucosal damage evoked by indomethacin and on gastric acid secretion. Following pylorus-ligation, indomethacin [20 mg/kg] was given subcutaneously and rats received 2 ml of 0.15 N HCI into their stomachs. Immediately afterwards, the drugs under study were given by the subctaneous route. Rats were killed 4 h after pylorus-ligation, and the number of gastric mucosal lesions were noted, their severity calculated and gastric acid secretory responses determined. The selective 5-hydroxytryptamine [serotonin] reuptake inhibitors [SSRIs] fluoxetine and sertraline caused dose-related increase in the degree of gastric mucosal injury caused by indomethacin. Similar effects were seen on administration of the heterocyclic agent; trazodone. In contrast, the indomethacin-induced lesion scores were remarkably reduced in rats treated with the non-selective noradrenaline and, serotonin reuptake inhibitors; imipramine and amitriptyline. Gastric acid secretion was increased by fluoxetine and sertraline administration, but reduced in rats treated with imipramine or amitriptyline. It is concluded that in the rat, the SSRIs fluoxetine and sertraline and the atypical antidepressant, trazodone, potentiate gastric mucosal damage caused by indomethacin in the presence of acid in the stomach. These results also suggest that changes in gastric acid secretion are involved in the modulatory effects induced by antidepressant drugs on gastric mucosal injury

Evaluation of effects of extract from seeds of myristica fragrans on volume and acidity of stimulated gastric secretion. liver and kidney function

This study was conducted to observe the effects of extracts from the seeds of medicinal plant "Myristica fragrans" [which has documented calcium channel blocker] on volume and acidity of carbachol induced gastric secretion, liver and kidney function in fasting rabbits. Thirty rabbits of local breed were included in the study and they were divided into three equal groups. Group A was injected with Carbachol. Group B was injected with extract and carbachol and group C was injected only extract and liver and kidney function was determined. The drugs and extract were injected intraperitoneally. It was observed that the extract inhibited volume, free and total acidity of gastric secretion in group B. This inhibition was statistically highly significant for all the three parameters [P< 0.001]. It was also noticed that there were non significant changes in liver function and kidney function test before and after 45 days treatment with extract in group C. It is concluded that the extract is an excellent inhibitor of gastric acid secretion and can be safely used for peptic ulcer and other diseases which need calcium channel blockers for their treatment. This will also enable a lay man to use the crude drug obtained from easily available local plant

Gastric pH and Helicobacter pylori Infection in Patients with Liver Cirrhosis / 대한간학회지

BACKGROUND/AIMS: Data from previous studies on gastric acid secretion and the prevalence of H. pylori in liver cirrhosis patients remain poorly defined. H. pylori is a potential source of NH3, but the possible role of H. pylori in hepatic encephalopathy is not clear. The purpose of this study was to compare gastric acid secretion, the impact of H. pylori infection, and the production of NH3 between cirrhotic patients and healthy, matched controls. METHODS: Twenty-nine patients with liver cirrhosis (HBV, n=12; Alcohol, n=12; HCV, n=5) were matched with 33 healthy persons for age and sex. None of the patients or controls were being treated with antacids, H2-receptor blockers or proton pump inhibitors. The pH and NH3 concentration was measured in gastric juice obtained by endoscopy. H. pylori infection was diagnosed using the rapid urease test. The level of NH3 in venous blood was also measured. RESULTS: The average gastric pH was significantly higher in cirrhosis patients compared to controls (3.91 vs. 2.99, P4) was significantly greater in cirrhosis patients (45 vs. 21%, P<0.05). In contrast, the prevalence of H. pylori infection (62% vs. 58%) and gastric NH3 concentrations (3.4 vs. 3.3 mM/L) were similar between both groups. However, venous NH3 levels were significantly higher in cirrhotics than in controls (63.1 vs. 25.2 micro M/L, P<0.05). The patients with H. pylori infection had significantly higher gastric NH3 concentration (3.8 vs. 1.6 mM/L) and gastric pH (3.87 vs. 2.76, P<0.05) than those without infection, but no significant difference in venous NH3 levels were detected (39.6 vs. 48.1 micro M/L). In patients with cirrhosis, the presence of H. pylori infection was not correlated with either gastric or blood NH3 levels. CONCLUSIONS: The gastric pH of liver cirrhosis patients is higher than that of controls and a larger proportion of cirrhotic patients have hypochlorhydria. The prevalence of H. pylori in liver cirrhosis patients was similar to that in controls and no correlation was found between gastric and blood NH3 levels. Thus, H. pylori infection does not seem to play a major role in generation of elevated NH3 associated with hepatic encephalopathy.