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Biomedical subjects

C H Cho

Publications and source records attributed to C H Cho.

At least 217 records · Page 12Linked to original sources
PubMed1986

Effects of verapamil, carbenoxolone and N-acetylcysteine on gastric wall mucus and ulceration in stressed rats.

The effects of verapamil on gastric wall mucus and ulceration were studied in rats which were restrained and exposed to 4 degrees C (stress). Stress for 2 h significantly depleted stomach wall mucus and produced marked gastric glandular ulcers. Verapamil pretreatment (2, 4, 8 or 16 mg/kg), injected intraperitoneally 30 min before experimentation, significantly prevented stress-induced mucus depletion and gastric ulceration; however, it did not itself influence stomach wall mucus levels in nonstressed animals. Intragastric administration of carbenoxolone (100 or 200 mg/kg), also given 30 min before stress, exhibited similar actions as verapamil. A 15% solution of N-acetylcysteine (10 ml/kg), given orally, strongly decreased the mucus content in both nonstress and stress conditions; it induced ulcers in nonstressed rats, and worsened stress ulceration. These effects were not reversed by verapamil pretreatment. The influence of multiple-dose pretreatment with verapamil or carbenoxolone on mucus content and ulceration in the gastric glandular mucosa during stress is also discussed. It is concluded that gastric wall mucus depletion is likely to play an important role in stress ulcer formation; the antiulcer action of verapamil could partly be due to the preservation of mucus.

Acetylcysteine↗
PubMed1986

Effects of carbenoxolone sodium on gastric and duodenal mucus synthesis in mice.

Using the method of staining mucus with Alcian blue and destaining it with magnesium chloride, it was found that intragastric administration of carbenoxolone in mice did not significantly affect duodenal mucus synthesis at doses which remarkably increased gastric mucus synthesis. However, in vitro study showed that carbenoxolone significantly stimulated both gastric and duodenal mucus synthesis. It is suggested that carbenoxolone may also effectively increase mucus synthesis and probably accelerate ulcer healing in the duodenum if sufficient amounts can escape gastric absorption and reach this region.

Alcian Blue↗
PubMed1986

Protection by zinc sulphate against ethanol-induced ulceration: preservation of the gastric mucosal barrier.

The aetiology of ethanol-induced gastric ulceration, and its interaction with zinc, were studied in rats. Oral administration of ethanol (40, 50 or 80%) to conscious rats reduced the stomach mucus content and increased gastric ulcer formation in a concentration-dependent manner. Histological examination indicated that mucus, both on the surface and within the epithelium, was depleted because of epithelium being shed from the gastric mucosa. Zinc sulphate abolished mucus loss and ulcer formation in the ethanol-treated animals. Using an ex-vivo gastric chamber preparation in anaesthetised animals, it was found that an ethanol (50%)-HCl (100 mmol/l) solution produced severe glandular haemorrhagic ulceration, elevated Na+, K+ and protein levels in the luminal solution, and reduced the H+ content in this fluid. Zinc sulphate pretreatment dose-dependently prevented all these changes. On the other hand, prostaglandin E2 (PGE2) administration only antagonised ethanol ulceration and H+ loss from the chamber; it did not significantly influence the Na+ and K+ fluxes and protein leakage into the luminal solution. It is concluded that the antiulcer mechanisms of zinc sulphate and PGE2 may be different. Protection by the former drug could be due partly to preservation of mucus adhering to the gastric mucosa. The possibility of the membrane-stabilising action of zinc contributing to the observed effects is also discussed.

Animals↗
PubMed1986

Effects of H2-receptor antagonists on the rat liver after partial hepatectomy or carbon tetrachloride-induced hepatic injury.

A total of 512 male rats were used to investigate the effects of H2-receptor antagonists on the liver after two-thirds hepatectomy or after carbon tetrachloride (CCl4)-induced hepatic injury. The serum aminotransferase levels in hepatectomy rats were significantly elevated as compared with those of rats with the sham operation 1 and 2 days after the operation. However, there were no differences in the serum aminotransferase levels and liver regeneration rates among the groups of hepatectomy rats who were treated with saline, cimetidine, or ranitidine. The injections of cimetidine or ranitidine did not induce a significant increase in serum amino-transferase levels or increase the severity of liver cell necrosis in CCl4-treated rats, as compared with the CCl4-treated rats who received saline injection. Thus, our data indicate that H2-receptor antagonists do not inhibit liver regeneration in rats after two-thirds hepatectomy or exert a detrimental effect on the liver cell necrosis in rats after CCl4-induced hepatic injury.

Alanine Transaminase↗
PubMed1986

The influence of partial hepatectomy and carbon tetrachloride on rat stomachs.

Carbon tetrachloride (CCl4) injection, but not partial hepatectomy, significantly increased gastric acid secretion and ulceration in rats. Both procedures did not influence serum IgG levels, but markedly elevated serum alanine and aspartate aminotransferase activities. It appears that short-term liver injury produced by CCl4, but not hepatectomy, adversely affects rat stomachs.

Alanine Transaminase↗
PubMed1985

The effect of nicotine on ethanol-induced gastric ulcers in rats.

Nicotine, in concentrations of 5 and 25 micrograms/ml drinking water, given ad libitum for 10 days, dose-dependently increased lesion formation and worsened ethanol-induced ulceration in rat stomachs. Daily fluid intake and b.wt gain were not adversely affected by nicotine pretreatment.

Animals↗
PubMed1985

The influence of verapamil on the gastric effects of stress in rats.

The influence of verapamil on stress- or bethanechol-induced gastric effects was investigated in rats. Intraperitoneally injected verapamil (1, 2 or 4 mg/kg), given 30 min beforehand, dose-dependently prevented gastric glandular ulceration, mast cell degranulation and the increased stomach wall contractions evoked by restraint at 4 degrees C for 1 h. Gastric acid secretion, as well as ulceration in both the forestomach and glandular segment, produced by subcutaneously-injected bethanechol (3.2 mg/kg) were also inhibited. It is concluded that decreased amine release from the mast cells, stomach wall relaxation and reduced gastric acid were responsible for the ulcer-antagonising effects of the calcium-entry blocker. The possible antiulcer actions of verapamil are discussed in the light of present knowledge regarding calcium involvement in the various mechanisms thought to contribute to the pathophysiology of stress ulceration in rat stomachs.

Animals↗
PubMed1985

The aetiology of gastric ulceration induced by electrical vagal stimulation in rats.

Histamine and serotonin levels in gastric secretion and the effects of pharmacological antagonists were studied in rats in which stomach ulceration was induced by electrical vagal stimulation. Electrical vagal stimulation (2 and 5 V) produced a graded increase in haemorrhagic glandular mucosal ulcers. NaHCO3 perfusion completely neutralised the increased acid output but failed to prevent ulceration. Atropine inhibited gastric mast cell degranulation as well as histamine and serotonin release. Diphenhydramine, atropine and sub-diaphragmatic vagotomy antagonised the increase in intragastric pressure. Diphenhydramine, cimetidine, atropine or vagotomy but not methysergide reduced ulcer severity. It is concluded that gastric acid and serotonin do not play an important role in glandular ulceration induced by electrical vagal stimulation. The lesions probably result from increased intragastric pressure and release of gastric histamine which stimulates H1 and H2 receptors in the stomach. The similarities between the aetiologies of glandular ulcers due to electrical vagal stimulation and to stress are also discussed.

Animals↗
PubMed1985

Sulphasalazine and experimental stress ulcers.

The effects of sulphasalazine on gastric ulceration induced by restraint at 4 degrees C (stress) for 2 h were studied in rats. Doses of 63 or 125 mg/kg s.c., which had no effect on stomach wall prostaglandin E2 (PGE2) levels, prevented stress ulceration but not the lesions produced by indomethacin. Stress significantly increased gastric glandular mucosal PGE2 levels. Indomethacin pretreatment (20 mg/kg, p.o.) markedly reduced PGE2 levels in the same region of the stomachs, and worsened stress-induced lesion formation. Pretreatment with sulphasalazine of animals given indomethacin and then subjected to stress did not appear to affect the indomethacin component of indomethacin-stress ulceration. Oral administration of PGE2 200 micrograms/kg significantly elevated gastric PGE2 levels, but had no effect on stress ulceration. It appears that neither the antiulcer activity of sulphasalazine nor stress-induced ulceration is associated with gastric tissue PGE2 increase or decrease, respectively. The protective mechanism may result from the ability of sulphasalazine to inhibit lipoxygenase activity.

Administration, Oral↗
PubMed1985

The effects of zinc sulphate on hypercholesterolaemia induced by cholesterol-choleate in rats.

The effects of zinc sulphate on cholesterol-choleate-induced hypercholesterolaemia were studied in rats. Zinc sulphate (20 or 40 mg/kg, p.o. once daily for 5 days) administration, which raised serum zinc levels, significantly increased bile acid secretion and lowered high-density lipoprotein-cholesterol (HDL-C) levels in the serum. Cholesterol-choleate, given by the same route and schedule, markedly elevated serum total cholesterol level, but decreased serum HDL-C concentration. Bile acid in serum and in bile was also increased, but these changes were inhibited by zinc sulphate pretreatment. Zinc sulphate also worsened the decrease in HDL-C and slightly prolonged the elevation in total cholesterol produced by cholesterol-choleate administration. It is concluded that the moderate increase in serum total cholesterol level by zinc sulphate could be due to inhibition of hepatic metabolism of cholesterol to bile acid. The specific action of zinc ions on HDL-C metabolism is discussed.

Animals↗
PubMed1985

Effects of eight-week treatment with oral ranitidine on plasma level changes of gastrin, histamine and serotonin in duodenal ulcer patients.

The effects of eight-week ranitidine treatment on changes in plasma gastrin, histamine and serotonin levels, and in intragastric pH and urinary 5-hydroxyindoleacetic acid in duodenal ulcer patients were studied. Elevated plasma gastrin and histamine levels, as well as intragastric pH were found after four weeks of ranitidine treatment, only in patients whose ulcers had healed. Plasma serotonin and urinary 5-hydroxyindoleacetic acid levels decreased as drug treatment continued, and the falls were similar in patients whose ulcers healed or did not. It is suggested that the increases in plasma gastrin, histamine and serotonin levels could be due to gastric and duodenal acid reductions by ranitidine. However, the possibility of a direct action of the drug on their release is yet to be excluded.

Adult↗
PubMed1985

The effect of cold-restraint stress on gastric emptying in rats.

The effects of drug treatment and of cold-restraint stress (a method used to produce experimental stomach ulcers) on gastric emptying of a resin (colestipol-phenol red complex) were investigated in rats. Gastric emptying was decreased by intraperitoneal treatment with atropine (0.3 mg/kg) or verapamil (4 mg/kg), and enhanced by bethanechol (1.2 mg/kg). Stress by restraint at 4 degrees C for 2 hr markedly reduced gastric emptying; the pattern of effects of drug pretreatment in these stressed rats was similar to that seen in their nonstressed controls. Further experiments, with stress for 3 hr, revealed that the gastric emptying rate was triphasic; increasing in the first hr, returning to normal and then slowing in the third hr of stress. Initial increase in emptying rate was probably due to predominant vagal overactivity. Hypothermia and possibly other factors induced by cold-restraint stress could have subsequently depressed gastric motility.

Animals↗
PubMed1985

Serum concentration of pancreatic polypeptide in normal subjects and in peptic ulcer patients.

The present study evaluates the serum concentration of pancreatic polypeptide (PP) in normal male and female subjects of different ages (ranging from 20 to 69) and also in patients with peptic ulcers. The PP level rose with age and was higher in the male subjects (from the age of 30). Serum levels of the peptide in patients with gastric or duodenal ulcers were not significantly different from the normal subjects (age and sex matched with the diseased groups).

Adult↗
PubMed1985

A study on the aetiology of reserpine ulceration and the antiulcer action of solcoseryl in rat stomach.

The aetiology of reserpine-induced gastric ulcer formation and the antiulcer effects of solcoseryl were studied in rats. Intraperitoneal injection of reserpine produced severe ulceration, as well as mast cell and histamine depletion, in the gastric glandular mucosa. Mepyramine and cimetidine markedly antagonized the gastric lesions, but did not influence the reduced mast cell count; atropine pretreatment significantly inhibited both parameters. Intramuscular injection of solcoseryl lessened ulcer severity and prevented the decreased mast cell counts and histamine levels in reserpine-treated rats. However, the same dose of solcoseryl injected intraperitoneally was ineffective. Solcoseryl, irrespective of the route of administration, did not influence the gastric secretory activities of reserpine. It is concluded that reserpine ulceration is both cholinergic- and histamine-mediated, and that the antiulcer effects of solcoseryl appear to be due to prevention of histamine depletion in the gastric mucosa.

Actihaemyl↗
PubMed1985

Effects of zinc sulphate on ethanol- and indomethacin-induced ulceration and changes in prostaglandin E2 and histamine levels in the rat gastric glandular mucosa.

The effect of zinc sulphate on stomach ulceration produced by ethanol and indomethacin was examined in rats. Oral or intraperitoneal pretreatment with zinc sulphate (20 mg/kg, expressed as zinc ion) strongly prevented ethanol-, but not indomethacin-induced gastric glandular ulceration. Indomethacin given beforehand did not influence the protective action of zinc sulphate against ethanol-evoked lesions. Ethanol decreased histamine levels, whereas indomethacin reduced the prostaglandin E2 (PGE2) content in the gastric glandular mucosa. The alcohol also elevated the histamine content in gastric secretion. Zinc sulphate reversed the ethanol-induced changes in histamine levels in both mucosa and secretion, but did not modify PGE2 reduction by indomethacin. Zinc sulphate also antagonised protein leakage from the stomach following ethanol administration. It is concluded that gastric ulceration by the currently employed doses of ethanol and indomethacin is caused by different mechanisms. Zinc sulphate prevents histamine-mediated lesions produced by the alcohol, but not ulceration due to PGE2 depletion by indomethacin.

Animals↗