Effect of hygiene measures, water sanitation and oral rehydration therapy on diarrhea in children less than five years old in the south of Ivory Coast

BACKGROUND: Gastric sucrose permeability is a noninvasive marker that reliably increases in association with gastrointestinal injury due to use of nonsteroidal antiinflammatory drugs. Despite the effect of Helicobacter pylori infection on the gastric mucosa, in a previous study we were unable to demonstrate that H. pylori infection was associated with abnormal gastric sucrose permeability. Our goal in this study was to explore further whether H. pylori infection changed gastric permeability; therefore, we evaluated the effect of treatment of H. pylori infection on gastric permeability to sucrose and the relation of sucrose permeability to density of polymorphonuclear leukocytes. MATERIALS AND METHODS: Five hundred milliliters of a solution containing 100 gm of sucrose was ingested by the subject at bedtime. Overnight urine was collected and assayed for sucrose by high-performance liquid chromatography. Sucrose permeability was assessed both before and approximately 4 weeks after anti-H. pylori therapy. RESULTS: Seventeen asymptomatic H. pylori-infected volunteers participated; 8 were cured. Sucrose permeability was in the range commonly found in normal controls both before and after anti-H. pylori therapy (mean excretion, 76.3 mg; range, 13-171 mg). Gastric sucrose permeability correlated with the density of polymorphonulcear cell infiltration of the mucosa. Cure of the H. pylori infection was associated with a small but significant decrease in sucrose permeability (98.8 +/- 18 mg to 51.7 +/- 9.8 mg (p = .01). Sucrose permeability was greater in those with a high density of mucosal polymorphonuclear cells compared to those with lower scores (119.5 +/- 4 vs 71.4 +/- 13 for those with scores > or = 5 compared to scores < or = 4; p = .023). Failed therapy resulted in an increase in the mucosal density of polymorphonuclear infiltration and sucrose permeability (56.4 +/- 13 mg-99.7 +/- 19 mg pretreatment vs posttreatment, respectively; p = .031). CONCLUSION: H. pylori gastritis causes a small but measurable increase in gastric permeability to sucrose that may reflect epithelial transmigration of neutrophils.     

Effects of pancreatic polypeptide amylin on ulceration and acid gastric secretion

The effects of the pancreatic polypeptide amyline on ulceration and acid gastric secretion were studied in rat experiments. Pyloric ligation was used as a model of ulceration. Amyline administration caused significantly less gastric mucosal damage in response to pyloric ligation. The severity of gastric mucosal damage averaged 47 +/- 13 mm2 in the control group and 25 +/- 11 mm2 (p < 0.005). The rate of acid gastric secretion in the animals whose pylorus had been ligated as judged by the pH of gastric content was significantly higher than that in the controls (2.87 +/- 0.22 and 2.34 +/- 0.17 (p = 0.05). It is concluded that amyline has a noticeable effect on the gastric mucosa. It is suggested that suppressed acid gastric secretion, i.e. reduced influence of aggressive agents on the gastric mucosa, is a mechanism of antiulcerative action of the peptide.     

Therapeutic use of carminomycin in soft tissue sarcomas

Under endoscopic control, biopsy specimens were taken from the oxyntic gland area of the stomach before and after administration of pentagastrin, synthetic secretin, and 13-norleucine motilin (13-nle-motilin), respectively. In 29 volunteers, the basal rate of 14C-leucine incorporation into mucosal protein averaged 41.2 +/- 7.7 X 103 cpm/mg protein (mean +/- S.D.). One and 4 hours after s.c. administration of pentagastrin (6 mug/kg body weight), values were significantly increased (p less than 0.05) by 18.9 and 21.8%, respectively, with respect to the basal level. One hour after an intravenous shot of 2 CU per kg body weight of secretin, gastric mucosal protein synthetis was not substantially inhibited, whereas a 1-hour continuous i.v. infusion of 13-nle-motilin (0.4 mug/kg body weight, hr) significantly decreased 14C-leucine incorporation rates by 17.5% (p less than 0.05). In contrast to rats, 1 hour after s.c. pentagastrin, protein synthesis in human duodenal mucosa was not altered. From these results it may be concluded that pentagastrin has a trophic influence on gastric mucosa in man. Moreover, the data presented are compatible with the hypothesis that gastrin and motilin may be involved in the regulation of human gastric mucosal protein synthesis.     

Overexpressed nitric oxide synthase in portal-hypertensive stomach of rat: a key to increased susceptibility to damage?

BACKGROUND & AIMS: Portal hypertension predisposes gastric mucosa to increased injury. The aim of this study was to determine whether overexpression of constitutive nitric oxide synthase (cNOS) is responsible for increased susceptibility of portal-hypertensive (PHT) gastric mucosa to damage. METHODS: In gastric specimens from PHT and sham-operated rats, cNOS messenger RNA expression was determined by Northern blotting and cNOS protein expression by Western blotting, immunohistochemistry, and enzyme activity assay. Extent of ethanol-induced gastric mucosal necrosis, mucosal blood flow, and gastric NOS activity in PHT and sham-operated rats was determined after administration of N(omega)-nitro-L-arginine methyl ester (L-NAME) or saline. RESULTS: cNOS messenger RNA level, cNOS enzyme activity, and fluorescence signals for cNOS were increased significantly in PHT rats compared with controls. Inhibition of overexpressed cNOS by L-NAME (5 mg/kg) significantly reduced ethanol-induced mucosal necrosis and normalized blood flow in PHT gastric mucosa, whereas this dose of L-NAME significantly increased mucosal necrosis in sham-operated rats. CONCLUSIONS: Portal hypertension activates the cNOS gene with overexpression of cNOS protein in endothelia of gastric mucosal vessels. Excessive NO production by overexpressed cNOS may play an important role in the increased susceptibility of PHT gastric mucosa to damage.     

Ameloblastic fibroma: a fine-needle aspiration case report

The aim of this study was to determine the effect of portal hypertension (PHT) on gastric mucosal glycoproteins in rats. PHT was induced experimentally by partial ligation of the portal vein (PVL) in 20 male Wistar rats: 10 rats (PVL4 group) were analyzed after 4 weeks and the remaining 10 (PVL8 group) after 8 weeks. In another group of 10 rats (control group), sham operations were performed. The severity of gastric mucosal lesions was evaluated macroscopically by a gross ulcer index. The gross ulcer indices in the PVL groups were significantly higher than those in the controls (p < 0.05). Histomorphometric evaluation of the intraepithelial mucin content, with the periodic acid-Schiff-Alcian blue staining technique, confirmed a significant decrease in mucosal glycoprotein production in the PVL groups (p < 0.05). Quantitative changes in gastric mucosal hexosamines were also used for mucosal glycoprotein analyses, and the hexosamine content of the gastric mucosa in the control, PVL4 and PVL8 groups were 300.7 +/- 7.8, 177.2 +/- 4.9 and 169.1 +/- 3.5 micrograms/100 mg dried mucosa, respectively. The gastric mucosal hexosamine content was significantly lower in the PVL groups than in the control group (p < 0.05). No significant differences were observed between the two PVL groups in the above-studied parameters. These findings reveal that PHT causes a decrease in gastric mucosal glycoproteins in rats, and the decreased mucin content may weaken an important defensive factor of gastric mucosa. We suggest that gastric mucosal glycoproteins may play an important role in the pathogenesis of gastric mucosal lesions from PHT.     

Anemia increases gastric blood flow in noncirrhotic and cirrhotic patients

BACKGROUND: Previous studies in rats have demonstrated that anemia induces a significant increment in gastric mucosal blood flow. In the present study, we investigated whether chronic anemia induces similar changes in gastric blood perfusion in humans, and if this effect is also present in cirrhotic patients in whom gastric blood flow is usually increased in basal conditions. METHODS: Gastric mucosal blood perfusion was assessed by means of laser-Doppler flowmetry and reflectance spectrophotometry applied through the endoscope. RESULTS: Anemia significantly increases laser-Doppler signal in cirrhotic (2.3 +/- 0.11 vs 2.9 +/- 0.22 volts, p < 0.05) and noncirrhotic patients (1.71 +/- 0.15 vs 2.24 +/- 0.17, p < 0.05). In anemic patients the index of hemoglobin concentration of the gastric mucosa, assessed by reflectance spectrophotometry, was significantly decreased in cirrhotic patients (107.6 +/- 4.7 vs 95.5 +/- 3.3, p < 0.05) and noncirrhotic patients (93.9 +/- 4.1 vs 76.1 +/- 4.2, p < 0.01), whereas the index of oxygen saturation was increased (36.7 +/- 0.7 vs 40.4 +/- 1.4, p = 0.05; and 36.4 +/- 1.1 vs 43.2 +/- 1.9, p < 0.01, respectively). CONCLUSIONS: In conclusion, chronic anemia is associated with an enhanced gastric blood perfusion reflected by an increased laser-doppler signal and gastric mucosal oxygen index despite a decrease in gastric hemoglobin concentration. In cirrhotic patients, anemia promotes a further increment in its basal gastric hyperemia.     

Involvement of free radicals and histamine in the potentiating action of cigarette smoke exposure on ethanol-induced gastric mucosal damage in rats

Cigarette smoking has been associated with peptic ulcer diseases. We studied the effects of cigarette smoke exposure on ethanol-induced gastric mucosal damage and its relationship with vascular integrity and the possible role of free radicals and histamine. Male Sprague-Dawley rats were exposed to cigarette smoke followed by ethanol administration (70% v/v). Smoke exposure alone dose-dependently reduced basal blood flow and increased xanthine oxidase (XO) activity but superoxide dismutase (SOD) activity remained unaffected in gastric mucosa. Cigarette smoking followed by ethanol administration significantly potentiated mucosal lesion formation along with augmentation of the mucosal blood flow, vascular permeability and myeloperoxidase (MPO) activity. The potentiating effect of smoking on ethanol-induced gastric mucosal lesion and MPO activity was abolished by pretreatment with allopurinol, terfenadine or ranitidine. Terfenadine and ranitidine also reduced the increased mucosal blood flow and vascular permeability induced by smoking and ethanol combined. These findings suggested that cigarette smoke adversely affected the defense mechanisms of the gastric mucosa by reducing the mucosal blood flow which in turn led to ischemia and increased XO activity. Activation of XO together with histamine H1 and H2 receptors stimulation could lead to neutrophil aggregation and vascular damage. However, the potentiating action of cigarette smoke on ethanol ulceration is unlikely through reduction of SOD activity in gastric mucosa.     

Insulin sensitivity in pre-eclampsia

Gastric mucosal damage induced by haemorrhagic shock in the anaesthetized rat has been evaluated by studying changes in capillary-to-lumen clearance of fluorescein isothiocyanate (FITC)-labelled dextran. Haemorrhagic shock (20 min ischaemia + 20 min reperfusion) induced a significant increase in blood-to-lumen permeability to FITC-dextran of different molecular weight (10,000, 40,000 and 70,000) without modifying the macroscopic integrity of the gastric mucosa. The increase in vascular permeability was dependent on the time of administration of the tracer and was correlated with an elevation of the protein content of the gastric lumen. Intravenous administration of the secretagogue pentagastrin (20 or 50 micrograms kg-1 h-1) did not significantly modify the vascular permeability to dextran in control animals or in animals subjected to haemorrhagic shock. When the intraluminal pH was reduced by intragastric administration of acidic saline solution, only pH 1, which itself induced the appearance of macroscopic mucosal lesions, significantly increased vascular permeability to dextran, both in control animals and in animals subjected to haemorrhagic shock. These findings suggest that stress induced by haemorrhagic shock increases vascular gastric permeability to dextran, by an acid-independent mechanism, without affecting the macroscopic integrity of the gastric mucosa.     

Regional gastric pH measurement in horses and foals

The pH of the gastric mucosal surface and gastric content was measured in 18 foals (mean age: 20 days) and 27 horses (mean age: 2.9 years) with a pH electrode passed through an endoscope biopsy channel. A reference electrode was attached to a shaved area on the neck. pH Measurements of the gastric mucosal surface at the dorsal squamous fundus (SF), squamous mucosa adjacent to the margo plicatus (MP), glandular fundus (GF) and the fluid or feed contents of the stomach were recorded in duplicate for each animal. In adult horses, the SF pH was greatest (5.46 +/- 1.82), with a decreasing pH ventrally toward the MP (4.12 +/- 1.62), to the glandular fundic mucosa (3.09 +/- 1.90), and fluid contents (2.72 +/- 1.86). The differences in pH at each site within the stomach were significant (P < 0.05). In foals, mean pH measurement of the SF was 4.88 +/- 1.30, the MP was 4.92 +/- 1.29, the GF was 2.10 +/- 1.45, milk and fluid contents was 1.85 +/- 0.53 (six foals), and feed contents was 3.39 +/- 1.77 (12 foals). The pH of the SF and MP were significantly greater (P < 0.05) than that of feed contents, which was significantly greater (P < 0.05) than that of the glandular mucosal surface and fluid contents. The results indicate a dorsal to ventral pH gradient of the gastric mucosal surface in adult horses, and that gastric acid secretion is competent in young foals.     

Development of photosynthetic electron transport in greening barley

Oxygen tension and potential difference were measured in the gastric mucosa of anesthetized dogs with an ultramicroelectrode technqiue while total blood flow and arteriovenous oxygen content difference were measured. In the control period, measurements were: gastric blood flow, 102.4 +/- 3.0 ml per min per 100 g of tissue; calculated oxygen consumption, 2.4 +/- 0.1 ml per min per 100 g of tissue; intracellular oxygen tension, 15.0 +/- 0.6 mm Hg; and intracellular potential difference, -50.8 +/- 1.5 mv. When gastric blood flow was reduced 50% by tourniquet ischemia, oxygen tension decreased 20% (P less than 0.05) but electrical potential and oxygen consumption did not change. When blood flow was reduced 75%, oxygen tension and potential difference decreased significantly, 60% and 35%, respectively, but oxygen consumption was unchanged. Zero blood flow reduced oxygen tension, electrical potential, and total oxygen consumption to zero; release of the arterial tourniquet allowed them to return to control levels. The critical oxygen tension at which the electromotive force generated by the gastric mucosal cells was reduced averaged 9 mm Hg. This suggests that safety factors exist in the gastric circulation which permit a 60% reduction in total gastric blood flow to occur before an insufficiency of intracellular oxygen begins to limit cellular metabolism within the mucosa.     

Luminal acid increases apical cell membrane resistance in isolated Necturus antral mucosa

BACKGROUND & AIMS: The gastric mucosa must have efficient protective mechanisms to maintain physiological intracellular pH. The aim of this study was to investigate the effect of low luminal pH on apical membrane permeability. METHODS: Chambered Necturus antral mucosa was perfused with Ringer's/95% O2-5% CO2 at pH 7.25. The mucosal side was exposed to pH 4.0-2.0 with four microelectrodes placed in surface cells. Two-dimensional cable analysis was used to measure apical, basolateral, and shunt resistances. In some experiments, liquid sensor pH or Na(+)-selective microelectrodes were used. RESULTS: Luminal acidification hyperpolarized apical cell membrane potential and increased apical cell membrane resistance from 21.3 +/- 2.6 (pH 7.25) to 38.0 +/- 2.3 k omega.cm2 (pH 3.0; n = 8). The increase in apical cell membrane resistance was preceded by transient intracellular acidosis from 7.32 +/- 0.07 (pH 4.0) to 7.23 +/- 0.06 (pH 3.0; n = 6). Similar intracellular acidosis (provoked by NH4+ prepulse) failed to cause the effects observed with luminal acid. The increase in apical cell membrane resistance caused by luminal acid was eliminated when N-methyl-D-glucamine+, but not Na+, was substituted for all cations in the luminal solution. CONCLUSIONS: Luminal acidification (pH 3.0-2.0) closes apical amiloride-blockable Na+ channels. Protons are probably able to pass and even block these channels, but their effect in closing the channels does not occur intracellularly.     

Endogenous vasopressin increases acute endotoxin shock-provoked gastrointestinal mucosal injury in the rat

Administration of a low dose of endotoxin (from Escherichia coli, 3 mg kg(-1), i.v.), which does not affect vascular permeability or blood pressure over 1 h, leads to the release of endogenous vasopressin and damage to the mucosal microvasculature. Thus, endogenous vasopressin could be involved in septic shock. In the present study, we investigated the role of endogenous vasopressin in gastrointestinal mucosal injury induced by acute endotoxin shock, which was generated in rats by administering a high dose of E. coli endotoxin (50 mg kg(-1), i.v.). Tissues were removed 15 min after endotoxin. The vasopressin V1 receptor antagonist, d[CH2]5Tyr[Me]arginine-vasopressin (0.2-1 microg kg(-1), i.v.), was injected 10 min before endotoxin. Monastral blue (30 mg kg(-1), i.v.), which stains damaged vasculature, was injected 10 min before autopsy. Endotoxin reduced systemic arterial blood pressure (from 115+/-5 to 42+/-4 mmHg), generated macroscopic and microvascular injury, and elevated plasma vasopressin levels (from 3.4+/-0.2 to 178+/-16 pg ml(-1)). The vasopressin V1 receptor antagonist reduced this macroscopic injury, and in the vasopressin-deficient Brattleboro rat a similar reduction of gastrointestinal mucosal damage was found. Substantial decreases in endotoxin-induced microvascular damage were observed in each tissue, e.g., the gastric Monastral blue staining was reduced by 47+/-3% and 96+/-3% (P < 0.01) after vasopressin V1 receptor antagonist treatment and in Brattleboro rats, respectively. Vasopressin, acting through its V1 receptors, thus appears to be involved in acute endotoxin shock-provoked gastrointestinal injury.     

The dynamics of pAL2-1 homologous linear plasmids in Podospora anserina

We have investigated the properties of the newly synthesized proton-pump inhibitor, 3-butyryl-8-methoxy-4-[(2-thiophenyl)amino]quinoline (YJA20379-6), on gastric mucosal proton-pump (H+/K+-ATPase) activity, gastric acid secretion and gastroduodenal lesions in experimental rats. YJA20379-6 markedly inhibited H+/K+-ATPase activity in rabbit isolated gastric mucosal microsomes, confirming its classification as a proton-pump inhibitor. The inhibitory efficacy of YJA20379-6 on the proton pump was approximately 14-times higher than that of omeprazole at pH 7.4. YJA20379-6 given intraduodenally had a potent inhibitory effect on gastric secretion in pylorus-ligated rats (ED50 22.9 mg kg(-1)) but was less active than omeprazole. Pretreatment of rats with YJA20379-6 dose-dependently protected the gastric mucosa from damage induced by water-immersion stress, indomethacin and absolute ethanol, and the duodenal mucosa from damage induced by mepirizole. Repeated administration of YJA20379-6 also dose-dependently accelerated the spontaneous healing of acetic acid-induced gastric ulcers. These results suggest that YJA20379-6 has potent anti-secretory and anti-ulcer effects which are exerted by suppression of H+/K+-ATPase activity in gastric parietal cells. YJA20379-6 might be useful for the clinical treatment of peptic ulcer diseases.     

Effects of erythrocyte lysate of different incubation times on intracellular free calcium in rat basilar artery smooth-muscle cells

The effects of 5-hydroxytryptamine (5-HT) on ethanol-induced gastric mucosal damage and on epithelial and vascular integrity were investigated. Male Sprague-Dawley rats were administered with 5-HT (5 or 10 mg/kg, IP) 30 min prior to the challenge with ethanol (40% v/v, 10 ml/kg, PO). 5-HT dose dependently aggravated ethanol-induced injury in the gastric mucosa. Both xanthine oxidase (XO) and myeloperoxidase (MPO) activities in the mucosa were significantly increased with the high dose of 5-HT, which also potentiated the elevation of these enzyme activities by ethanol. However, the mucosal superoxide dismutase activity was left unaltered. In neutropenic (antineutrophil serum-treated) animals, the ethanol-induced gastric mucosal injury was significantly ameliorated, with or without the pretreatment of 5-HT (10 mg/kg). In addition, the effect of 5-HT on the activity of MPO, but not of XO, was also attenuated in these animals. In the ex vivo gastric chamber study on pentobarbital-anesthetized animals, volume of gastric secretion was significantly decreased in the 5-HT-treated groups, with further reduction after ethanol incubation. Transmucosal potential difference (PD) was significantly reduced in 5-HT-treated rats, which also potentiated the ethanol-induced drop in PD. Nevertheless, 5-HT dose dependently increased mucosal vascular permeability and further enhanced during ethanol incubation. These findings suggest that 5-HT adversely affects the defense mechanisms of the gastric mucosa by reducing the secretory function of the mucosal cells and to weaken the epithelial and vascular integrity. Neutrophil activation appears to be responsible for the detrimental effects of 5-HT partly through the elevation in MPO activity. The increase in mucosal XO activity by 5-HT may induce free radical production and possibly modulate the ulcerogenic processes.     

Comparative clinical study of cefonicid, chloramphenicol, and penicillin in community-acquired pneumonia

Telomere length in human somatic cells gradually decreases with the number of cell divisions and is regarded as a marker of somatic cell turnover. Mucosal cells of the affected colon show rapid turnover in individuals with active ulcerative colitis (UC). Telomere length was determined by Southern blot analysis of terminal restriction fragments (TRFs) from the colonic mucosa of 17 patients with UC in remission, two of whom showed dysplasia, and 17 control subjects without colitis. For each individual, mean TRF length was compared between rectal mucosa and unaffected cecal mucosa. The mean TRF length of the rectal mucosa was significantly less than that of cecal mucosa in UC patients (7.87 +/- 0.36kb versus 8.77 +/- 0.21 kb; P = 0.0015, Wilcoxon signed rank test), whereas no significant difference was detected in the control subjects. The extent of telomere shortening was 10.6 +/- 3.35% in UC patients, compared with 0.8 +/- 0.64% in noncolitis controls (P = 0.0024, Mann-Whitney U-test). Four UC patients, two of whom had dysplasia, showed telomere shortening of more than 20% in the rectal mucosa. These observations suggest that telomere shortening in the colonic mucosa of individuals with UC may represent the history of mucosal inflammation during disease of long duration, and that it may contribute to aneuploidy in UC.     

The effect of dopamine and PGI2 on indomethacin and alcohol-induced gastric lesions in rats of various ages in relation to gastric vascular permeability and HCl secretion

Gastric lesions induced by indomethacin (20 mg.kg-1 i.p.) and ethanol (1 ml 95% intragastrically) were studied in rats after a 24 hour fast. The size of gastric lesions was correlated with gastric HCl secretion and with gastric vascular permeability (determined from the Evan's blue concentration in the gastric tissue after its i.v. administration). These parameters were also studied in rats pretreated with either PGI2 (5 micrograms.kg-1) or dopamine (0.5 mg.kg-1). It was found that in 12-months old rats the gastric lesions were significantly higher compared with the 3-month old group. PGI2 and dopamine significantly decreased gastric lesions in the 3-month rats but not in 12-month old rats. Both indomethacin and ethanol increased gastric vascular permeability in both age groups. It was observed that the decrease of gastric lesions after pretreatment with PGI2 and dopamine in the 3-month old rats was followed with decreased gastric vascular permeability and HCl secretion. On the other hand the increased susceptibility of the gastric mucosa due to indomethacin in the 12-month old rats was followed by a decrease of HCl secretion. PGI2 or dopamine had any effect on the 12-month old rats. These results show that susceptibility of gastric mucosa to PGI2 and dopamine is dependent on age. (Fig. 3, Ref. 31.)     

Bleeding in portal hypertensive gastropathy evaluated in terms of gastric mucosal microcirculation and coagulation-fibrinolysis system

Gastric intramucosal bleeding in portal hypertensive gastropathy was investigated in terms of gastric mucosal microcirculation, coagulation-fibrinolysis factors, and local fibrinolysis in patients with liver cirrhosis. The gastric mucosa was examined by endoscopy, and the patients were classified into two groups with or without bleeding. Gastric mucosal blood flow was measured simultaneously with coagulation-fibrinolysis factors or local fibrinolysis in both groups. As gastric mucosal blood flow, the gastric mucosal blood volume (IHb) and the oxygenated hemoglobin concentration (ISO2) were determined by the organ reflection spectrum method. Coagulation-fibrinolysis factors were measured in the blood. For evaluation of local fibrinolysis, gastric biopsy specimens were placed on a standard fibrin plate, and the fibrinolysis area was measured. Compared with the non-bleeding group, the bleeding group showed increased IHb and decreased ISO2 (p < 0.05), suggesting marked congestion of blood flow. Gastric intramucosal bleeding was frequently observed in patients with marked congestion of blood flow and markedly abnormal values of coagulation-fibrinolysis factors. Gastric local fibrinolysis was also significantly enhanced in the bleeding group (p < 0.05). In addition, local fibrinolysis was correlated positively with the gastric mucosal blood volume (r = 0.68, p < 0.05) and negatively with the oxygenated hemoglobin concentration (r = -0.58, p < 0.05). These results suggest the following mechanism of gastric mucosal bleeding in liver cirrhosis and portal hypertension. Congestion of gastric mucosal blood flow is present in liver cirrhosis and portal hypertension. An increase in the microvascular pressure and hypoxia cause release of tissue plasminogen activators from gastric mucosal cells and vascular endothelial cells. As a result, gastric local fibrinolysis is enhanced, causing gastric mucosal bleeding.     

Assisted conception: current techniques and outcome

PURPOSE: To determine whether ingestion of a tooth whitener containing 6% hydrogen peroxide as bleaching agent affected the gastric mucosa of adult, female laboratory rats. MATERIALS AND METHODS: Thirty-six fasting rats were intubated with a single bolus (5 g/kg body weight) of the tooth whitener Natural White which contains 6% hydrogen peroxide. Thirty-two control rats received deionized water. Rats were necropsied 15 minutes, 2 hours, 1 and 2 weeks after whitener ingestion. The gastric mucosa was examined histologically and blood hematocrit, glucose, BUN, and bilirubin measured. RESULTS: Six of the 36 rats died within 2 hours of receiving whitener. Within 15 minutes of whitener ingestion, stomachs were grossly bloated with gas. Histological observation showed that gastric mucosal cells were vacuolated and gastric glands dilated. After 2 hours, gastric epithelial and glandular cells had sloughed off into the gastric lumen. Mean blood glucose and hematocrit were significantly (P < 0.05) elevated (233 +/- 41 mg/ml and 50.5 +/- 0.9%) over mean control values (129 +/- 8 mg/ml and 42.8 +/- 2.4%). Within 1 week, the stomachs of experimental rats were no longer bloated, the gastric mucosa appeared normal histologically, but mean blood hematocrit was significantly (P < 0.05) decreased (38.0 +/- 1.5%) from mean control value (43.3 +/- 0.5%). There were no significant differences in mean blood values 2 weeks after whitener ingestion.     

Mucosal ulceration in isolated amphibian stomachs in vitro. Roles of nutrient HC03- and endogenous prostaglandins

We examined the effects of nonsteroidal anti-inflammatory drugs (NSAIDs) on mucosal ulceration in isolated bullfrog stomachs and investigated the roles of endogenous prostaglandins (PGs) and nutrient HCO3- in the mucosal protection in vitro. Gastric sacs were prepared by separation from the muscle layer and incubation for 1-8 h in HCO3--Ringer's solution gassed with 95% 02/5% CO2 or PO3(-)4-Ringer's solution gassed with 100% 02 in the presence of histamine (1 x 10(-4) M). Under these conditions, multiple ulcers developed in the mucosa only when the gastric sacs were incubated in HCO3--free nutrient solution; both the number and severity of ulcers increased with time and reached a maximum after 6 h of incubation. Luminal pH was decreased because of stimulation of acid secretion by histamine, irrespective of whether the mucosa was bathed in Ringer's solution with or without HCO3-, while gastric potential difference was reduced only in the mucosa bathed in HCO3--free nutrient solution. 16,16-Dimethyl PGE2 added to the nutrient side significantly reduced the number of ulcers developed in the mucosa bathed in HCO3--free nutrient solution. In contrast, indomethacin and aspirin, but not salicylate, caused ulceration even in the mucosa bathed in HCO3--nutrient solution. Histamine-induced acid secretion was reduced by 16,16-dimethyl PGE2 but not affected by these NSAIDs. In conclusion, ulceration of the isolated gastric mucosa in the presence of acid depends upon either a deficiency of endogenous PGs or a lack of nutrient HCO3-/CO2.