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Biomedical subjects

C H Cho

Publications and source records attributed to C H Cho.

261 records · Page 15Linked to original sources
PubMedDate not supplied

Ethanol-induced gastric mucosal damage in the rat with Taenia-stimulated hypertrophic gastropathy.

The susceptibility to ethanol-induced lesions was studied in rats with experimental hypertrophic gastropathy, in order to examine the nature of gastric mucosal resistance in this condition. Acute erosions were induced by a standard per os method of administration with graded concentrations of ethanol; underlying mucosal hypertrophic gastropathy was induced by infection with Taenia taeniaeformis. The gastric mucosal content of histamine and serotonin was also assessed. Hypertrophic gastropathy was characterized by mucus cell hyperplasia, greatly increased stomach weight, increased mucosal content of histamine, and no effect in resistance to gastric injury induced by graded doses of ethanol. Correlated changes in serotonin content with treatment were not observed, but mucosal histamine content was correlated inversely with ethanol administration in both parasite-infected and non-infected rats. This model of hypertrophic gastropathy could be of interest to study the pathogenesis of hypertrophic gastropathy and its response to known injurious agents.

Animals↗
PubMedDate not supplied

The effect of misoprostol, omeprazole and sucralfate on nicotine- and ethanol-induced gastric injury and gastric mucosal blood flow: a comparative study.

Nicotine, which is thought to be responsible for part of the pharmacological effect of smoking, exacerbates gastric mucosal injury in rats. The effects of misoprostol (12.5 micrograms to 100 micrograms), omeprazole (12.5 mg to 100 mg) and sucralfate (50 to 400 mg) on gastric mucosal blood flow and mucosal injury induced by nicotine were studied in an ex vivo gastric chamber preparation in rats. Rats were pretreated with nicotine (25 micrograms/mL orally) for 10 days and ethanol was added to the gastric chamber preparation. Laser Doppler flowmetry was used to measure the gastric mucosal blood flow and mucosal damage (ulcer index) was assessed by the area of haemorrhagic lesions. The ulcer index was significantly higher in rats pretreated with nicotine. Treatment with misoprostol and omeprazole lowered the ulcer index significantly compared with controls. The peak and summation blood flows were lower in nicotine-treated rats but failed to reach statistical significance. The peak blood flow (blood flow at 45 min) and the summation blood flow were significantly higher with all doses of sucralfate, misoprostol and omeprazole than in controls (P less than 0.05). The increase in gastric mucosal blood flow was significantly higher with sucralfate and misoprostol than with omeprazole. We conclude that sucralfate, misoprostol and omeprazole prevent nicotine- and ethanol-induced gastric mucosal damage and are accompanied by an increase in gastric mucosal blood flow. This indicates that smoking exacerbates gastric mucosal injury and that cytoprotective and site-protective agents can reduce injury by these noxious agents.

Animals↗
PubMedDate not supplied

The role of the vagus nerve in the protective action of acid inhibitors on ethanol-induced gastric mucosal damage in rats.

The role of vagus in the actions of different acid inhibitors on ethanol-induced gastric damage and mucosal blood flow (GMBF) changes was studied in anaesthetized rats, using an ex vivo stomach chamber preparation. Subdiaphragmatic bilateral vagotomy decreased the basal gastric acid secretion and GMBF; it also intensified ethanol-evoked lesions in the glandular mucosa. Misoprostol, omeprazole and cimetidine produced a similar degree of reduction in acid output. Misoprostol given subcutaneously (s.c.) (50 micrograms/kg), or added to the incubation solution (12.5 micrograms) for 15 min, markedly prevented ethanol-induced lesion formation and reduction in GMBF. The reversing effect of s.c. injection of misoprostol on either lesion formation or on GMBF reduction was attenuated by vagotomy. Omeprazole protected against lesion formation only when present in the incubation solution (12.5 mg) of ex vivo chamber preparations of both vagus-intact and vagotomized animals, but the effect was significantly less in the latter group. The drug also prevented the depressive action of ethanol in vagus-intact animals. Cimetidine pretreatment (50 mg s.c. or 12.5 mg in incubation solution), however, did not modify the effects of ethanol on lesion formation and the GMBF. The findings indicate that the three different types of acid inhibitors exert different actions on ethanol-induced gastric mucosal damage, although they produced similar inhibition of acid output. Vagotomy lowers the GMBF and attenuates the antiulcer action of misoprostol and omeprazole, especially when the drugs are given by the parenteral route.

Animals↗
PubMedDate not supplied

A correlative study on the mechanism of adaptive cytoprotection against ethanol-induced gastric lesion formation in rats.

The protective effect of mild irritants against the subsequent gastric injury induced by necrotizing agents has been termed 'adaptive cytoprotection'. In this study, the possible pathway and mechanisms of adaptive cytoprotection induced by 20% ethanol were investigated. An ex-vivo gastric chamber preparation was used. The gastric mucosa was exposed to 20% ethanol before subsequent administration of 100% ethanol 15 min later. Subdiaphragmatic vagotomy or drug pretreatment was carried out in order to elucidate the mechanisms of adaptive cytoprotection by 20% ethanol. The results showed that 20% ethanol pre-exposure significantly protected the gastric mucosa against damage caused by 100% ethanol. This protective action was completely abolished by atropine or lidocaine pretreatment, whereas vagotomy and hexamethonium failed to have a significant influence. The cytoprotective effect, however, was independent of the gastric secretory volume, titratable acid content, luminal soluble mucus level and gastric mucosal blood flow. Exposure of only half the gastric mucosa to the mild irritant resulted in the protection of both sides of the mucosa. All these findings indicate that the adaptive cytoprotection of 20% ethanol involves the participation of chemoreceptors and muscarinic receptors in the gastric mucosa. An internal enteric reflex arc, with transmission of signals within the gastric mucosa, may also contribute to the cytoprotective process of the mild irritant.

Adaptation, Physiological↗
PubMedDate not supplied

Gastric cytoprotection by amoxycillin in the rat.

Amoxycillin in combination with anti-ulcer agents has been shown to prolong duodenal ulcer remission. While this effect can be related to the eradication of Helicobacter pylori, it is not known if amoxycillin might possess cytoprotective properties. Protection against ethanol-induced gastric mucosal damage by intragastric instillation of amoxycillin suspension (prepared from capsule form) and solution (from injection form, 100% pure amoxycillin), and by intraperitoneal injection of amoxycillin solution was studied using an ex vivo gastric chamber in the rat. Intragastric and intraperitoneal administration of amoxycillin dose-dependently protected the rat gastric mucosa from damage by absolute ethanol. This protection was lost when the rats were pretreated with indomethacin. Gastric mucosal blood flow as measured by laser Doppler flowmetry and gastric acid output were unaffected by amoxycillin. Amoxycillin imparts gastric cytoprotection, and one possible mechanism is by the release of prostaglandins.

Amoxicillin↗
PubMedDate not supplied

Cigarette smoke increases apoptosis in the gastric mucosa: role of epidermal growth factor.

BACKGROUND/AIMS: Apoptosis is a common mechanism for the regulation of cell loss. It is associated with both tissue atrophy and metaplasia. Cigarette smoking has tremendous adverse effects on the stomach and also increases the risk of gastric cancer. This action may be through the change in apoptosis in the stomach. The aim of this study was to examine the effect of cigarette smoking on apoptosis in the gastric mucosa and the possible role of epidermal growth factor (EGF) in this action. METHODS: Gastric blood flow was assessed by the laser Doppler technique. Serum and gastric mucosal EGF levels were measured by RIA. Gastric mucosal apoptosis was determined using TdT-mediated dUTP-biotin nick end labeling (TUNEL). RESULTS: Cigarette smoke exposure decreased serum EGF which was accompanied by a reduction in gastric blood flow. Meanwhile, gastric mucosal cell apoptosis was increased. Administration of EGF (20 microg/kg i.v.) before each cigarette smoke exposure reversed these actions. Removal of salivary glands induced similar effects on the gastric blood flow, apoptosis, and serum EGF level as with cigarette smoke exposure. CONCLUSION: A reduction in serum EGF was involved in the decrease in gastric blood flow and increase in gastric mucosal apoptosis caused by cigarette smoking.

Analysis of Variance↗
PubMedDate not supplied

[The identification of high-risk pregnancy, using a simplified antepartum risk-scoring system].

This study was carried out to assess the problems with the pregnant women, and check out the risk-factors in the high-risk pregnancies, using a simplified antepartum risk-scoring system, which was revised from Edwards' scoring system to be suitable for Korean situation. This instrument was included 4 categories, demographic, obstetric, medical and miscellaneous factors. This survey was based on the 1300 pregnant women who were admitted, from Jan. 1, 1988, to May 31, 1990, Chung Ang Medical Center. Data were collected from June 25, 1990 to July 7, 1990. Data was analyzed by x2-test, F-test, Pearsons correction, using statistical package SAS in NAS computer system, KIST. The results of the study were as follows; 1. 1313 infants were deliveried of these 560 infants (42.7%) were born to mothers with risk-scores greater than 7, and 753 infants (57.3%) were born to mothers risk-scores less than 7. 2. Maternal age, parity, education level, of the demographic factors were significant relation statistically to identify the high risk pregnancies (X2 = 20.88, 42.87, 15.60 P less than 0.01). 3. C-section, post term, incompetent cervix, uterine anomaly, polyhydramnios, congenital anomaly, sensitized RH negative, abortion, preeclampsia, excessive size infant, premature, low birth weight infant, abnormal presentation, perinatal loss, multiple pregnancy, of the obstetric factors were significant relation statistically to identify the high risk-pregnancies. (chi 2 = 175.96, 87.5, 16.28, 21.78, 9.46, 8.10, 6.75, 22.9, 64.84, 6.93, 361.43, 185.55, 78.65, 45.52, P less than 0.01). 4. Abnormal nutrition, anemia, UTI, other medical condition (pulmonary disease, severe influenza), heart disease, V.D., of the miscellaneous and medical factors, were significant relation statistically to identify the high risk-pregnancies. 5. Premature, low birth weight infant, contracted pelvis, abnormal presentation, of the risk factors were significantly related with Apgar score at 1 & 5 minute after birth and neonatal body weight. 6. Apgar score at 1 & 5 minute after birth and neonatal body weight were significantly negative correlated with risk-score. 7. There were statistically significant difference between risk-score and Apgar score at 1 & 5 minute after birth, 3 group (0-3, 4-6, above 7), and neonatal body weight, 2 group (below 2.5 kg, the other group) (F = 104.65, 96.61, 284.92, P less than 0.01). 8. Apgar score at 1 & 5 minute after birth (below 7), and neonatal body weight (below 2.5 kg), were significant relation statistically with risk score. (chi 2 = 65.99, 60.88, 177.07, P less than 0.01) were 60.8%, 60%.(ABSTRACT TRUNCATED AT 400 WORDS)

Apgar Score↗
PubMedDate not supplied

Role of gastric glandular mucosal energy metabolism in cold-restraint gastric lesion formation.

The effects of cold and restraint and of some of the antiulcer drugs on adenosine nucleotide content in the gastric glandular mucosa were examined. A bioluminescence technique was used to measure the amount of ATP and its metabolites in gastric mucosal tissue. Cold-restraint produced gastric lesions and increased the gastric mucosal ATP. Verapamil pretreatment attenuated these lesions and further intensified the ATP increase in a dose-related manner. The ATP/ADP ratio and the Atkinson index were also elevated. Calcium gluconate produced similar effects. Atropine or EGTA pretreatment protected or worsened the gastric lesion, respectively, but did not have any influence on the changes in mucosal energy metabolism. Ranitidine pretreatment lessened the lesion formation but had no influence on the nucleotide content. These findings indicate that the metabolic rate of the gastric mucosa is suppressed during cold-restraint conditions; this depression is probably due to hypothermia and reduction of mucosal metabolism. The lesion-protecting mechanisms of the drugs do not seem to be mediated through their effects on mucosal energy metabolism. The oxygen- and ATP-sparing effects of verapamil may contribute partly to its gastro-protective effect.

Adenosine Diphosphate↗