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Biomedical subjects

C H Cho

Publications and source records attributed to C H Cho.

At least 235 records · Page 13Linked to original sources
PubMed1984

Study of the effects of insulin on the migration of Hymenolepis diminuta in rats.

The effects of insulin on worm (Hymenolepis diminuta) migration was studied. Insulin injection (20 U/kg, s.c.) significantly increased gastric acid output but did not affect the serotonin content of blood, intestinal lumen or worms. The drug produced, dose-dependently, posteriad migration of the worms in rats without pylorus-ligation but ligation of the pylorus prevented this migration. It is concluded that the hypersecretion of gastric acid induced by insulin is responsible for the posteriad migration of H. diminuta in rats.

Animals↗
PubMed1984

Pathogenesis of gastric ulceration produced by acetazolamide in rats.

The present experiment demonstrated that relatively high doses of acetazolamide (100 and 200 mg/kg s.c.) induced severe gastric hemorrhagic ulceration in rats. This ulceration was aggravated by oral administration of HC1, but was inhibited by NaHCO3. Further, the severity of ulceration was also decreased by pretreatment with methysergide, chlorpheniramine, or cimetidine. These protective effects were affirmed by an increase in serotonin and histamine released from the stomach after acetazolamide treatment. Acetazolamide injection also increased the protein level, but reduced the sialic acid content in the gastric secretion, indicating that the gastric mucosal barrier may have been damaged. Prostaglandin E2 content of the gastric mucosa was not affected by the drug; however, carbonic anhydrase activity was markedly reduced in a dose-dependent manner. Thus, it is suggested that the ulceration induced by acetazolamide is mainly due to the inhibition of carbonic anhydrase activity and mucus secretion. The increases in serotonin and histamine released may also have been contributing factors for gastric ulcer formation.

Acetazolamide↗
PubMed1984

Papain reduces gastric acid secretion induced by histamine and other secretagogues in anesthetized rats.

We studied the effect of papain on rats' gastric acid secretion and found that: 1. Feeding of latex of unripe papaya fruit significantly reduced gastric acid secretion induced by methacholine; 2. Feeding of crystalline papain in doses of 3.2 mg/kg reduced gastric acid secretion induced by histamine, methacholine and tetragastrin; 3. The reduction of gastric acid secretion was observed as early as 2 hours after papain feeding, lasted up to 48 hours, and waned within 96 hours; 4. Intraperitoneal injection of papain had no effect on acid secretion. These results led us to believe tha the effect of papain on gastric acid secretion is a local one acting directly on the gastric mucosa, and this local effect of a single dose of papain is reversible, causing no permanent damage to the mucosa.

Administration, Oral↗
PubMed1984

Study of the damaging effects of acetazolamide on gastric mucosa in rats.

The present study demonstrated that acetazolamide (100 and 200 mg/kg, s.c.) induced severe gastric hemorrhagic ulceration in rats. The ulceration was aggravated by oral administration of HCl, but was inhibited by NaHCO3. Furthermore, the severity of ulceration was also decreased by pretreatment with methysergide, chlorpheniramine, or cimetidine. These protective effects were accompanied by an increase in serotonin and histamine released from the stomach. Acetazolamide injection also increased the protein level but reduced the sialic acid content in the gastric secretion, indicating that the gastric mucosal barrier may have been damaged. Prostaglandin E2 content of the gastric mucosa was not affected by the drug; however, carbonic anhydrase activity was markedly reduced in a dose-dependent manner. Thus, it is suggested that the ulceration induced by acetazolamide is mainly due to the inhibition of carbonic anhydrase activity and mucus secretion. The increase in serotonin and histamine release also may have been the contributing factors for gastric ulcer formation.

Acetazolamide↗
PubMed1983

The lack of effects of somatostatin on gastric responses induced by electrical vagal stimulation.

The effects of somatostatin on ulcer formation, gastric acid secretion and histamine release were assessed during vagus nerve stimulation in rats. Direct electrical vagal stimulation significantly increased histamine release and acid output in gastric secretion but decreased mast cell counts in gastric glandular mucosa. Hemorrhagic ulceration on the gastric glandular mucosa was also observed. Somatostatin pretreatment (10 micrograms/kg) did not inhibit gastric ulcer formation, gastric acid secretion or histamine release induced by vagal stimulation. Cimetidine (an H2 blocker) pretreatment, however, significantly decreased gastric acid secretion as well as ulcer formation. The present study indicates the direct vagal stimulation increases gastric acid secretion and ulcer formation. These effects are partially histamine dependent. Somatostatin did not inhibit histamine release induced by vagal stimulation and reflects the inability of the drug to prevent ulcer formation and gastric output under these conditions in rats. However, the inhibition of basal gastric acid secretion produced by somatostatin might be useful clinically in humans.

Animals↗
PubMed1982

Circadian variation in the distribution of Hymenolepis diminuta (Cestoda) and 5-hydroxytryptamine levels in the gastro-intestinal tract of the laboratory rat.

The circadian migration of Hymenolepis diminuta in the small intestine of the rat may be correlated with a circadian variation in 5-hydroxytryptamine levels present in worm tissue, in the intestinal lumen, in the intestinal mucosa, with the amount of fold present in the small intestine and in arterial blood. 5-HT and food levels in uninfected animals were also determined. The 16.00 h stage in the circadian cycle marks both the commencement of host feeding, followed by rising 5-HT levels in both worm and host tissues, and initiation of an anteriad migration of worm biomass. It was found that 5-HT levels in the intestine of parasitized animals were significantly higher than in the intestine of uninfected controls. This is the first report of circadian variation in mucosal and luminal 5-HT levels. The similarity in the circadian patterns of worm migration and worm luminal, mucosal and blood 5-HT levels were striking. Fasting eliminated the circadian rise in intestinal 5-HT levels and the worms did not migrate. Luminal 5-HT levels were significantly lower in fasted animals than in the comparable rats fed ad libitum. When the intestine was ligatured at the pyloric sphincter, worm anteriad migration still occurred after feeding, indicating that the presence of exogenous food in the intestine is not a factor in the initial migration of the worms.

Animals↗
PubMed1981

Gastrointestinal ulceration in the guinea pig in response to dimaprit, histamine, and H1- and H2-blocking agents.

Histamine is known to induce gastric ulcers in guinea pigs after intraperitoneal administration and duodenal ulcers after repeated intramuscular administrations. This study was undertaken to clarify further the differential role of H1 and H2 receptor sites in respect to gastric and duodenal ulcer in the guinea pig. Groups of guinea pigs were treated with histamine, intraperitoneal (1.81 mg/kg intraperitoneal) or intramuscular (0.09 mg/kg intramuscular X 8 doses); the selective H2 agonist dimaprit (0.09-0.18 mg/kg X 8 doses intramuscular or 1.81-3.62 mg/kg intraperitoneal); NaCl, 154 mM (control); and the selective H1 and H2 antagonists, diphenhydramine (125 mg/kg X 2 doses, intramuscular) or cimetidine (50 mg/kg X 3 doses, intramuscular). Gastric and duodenal lesions were evaluated and residual gastric contents were analyzed. The selective induction of gastric or duodenal ulceration by histamine was confirmed, and the H2 agonist, dimaprit, has been shown to be ulcerogenic to the guinea pig duodenum by intraperitoneal or intramuscular administration. Diphenhydramine produced considerably more protection against histamine-induced gastric ulceration (62% decrease in incidence), while cimetidine was particularly effective in the prevention of histamine-induced duodenal ulcer (64% decrease in incidence). A differential role of histamine in the pathogenesis of gastric as opposed to duodenal ulcer is suggested by the present findings.

Animals↗
PubMed1981

Migration of Hymenolepis diminuta (Cestoda) and changes in 5-HT (serotonin) levels in the rat host following parenteral and oral 5-HT administration.

Changes in the distribution of the tapeworm Hymenolepis diminuta in the rat small intestine were studied for up to 3 h following intraperitoneal, intramuscular, subcutaneous, and oral administration of 5-HT. Changes in 5-HT levels in the arterial circulation, intestinal lumen, and in worm tissue were also monitored. In all cases following 5-HT administration there was an anteriad migration by H. diminuta. The extent of the migration was dose dependent, the higher the dose the more marked the migration response. Normal 5-HT levels in the parasitized gut are higher than those in uninfected animals. The pattern of increasing levels of 5-HT in worm tissue directly followed the increases in the intestinal lumen, suggesting that worm 5-HT was of host origin. Blood 5-HT level similarly followed luminal increases. It is suggested that the pharmacological action of 5-HT on H. diminuta resulting in worm migration is implemented through the regulation of helminth neuromuscular activity and the carbohydrate metabolism, as has been demonstrated in other parasitic worms.

Animals↗
PubMed1981

Effect of electrical vagal stimulation on migration of hymenolepis diminuta.

Stimulation of the left efferent vagal nerve (2 msec, 5 V, 10 Hz), for up to 60 min in rats infected with 11-day-old Hymenolepis diminuta induced anteriad migration of worm scolex and biomass in the small intestine. Ligation at the pyloric sphincter prior to vagal stimulation shortened the length of time before significant relocation occurred and increased the migrational response. The results support the hypothesis that work migration is mediated via vagal stimulation of gastrointestinal function, and is unrelated to actual feeding.

Animals↗
PubMed1980

Reserpine-induced gastric ulcers: protection by lysosomal stabilization due to zinc.

The effects of graded doses of zinc sulfate pretreatment on reserpine-induced gastric ulceration and on lysosomal fragility both in vivo and in vitro, were studied in rats. Reserpine treatment (5 mg/kg, i.p., 18 h before sacrifice) induced marked gastric glandular ulceration and elicited the release of free beta-glucuronidase from lysosomes in the gastric mucosa. A similar effect on release of this enzyme from isolated rat hepatic lysosomes was observed after in vitro incubation with reserpine. Zinc sulfate (22, 44 or 88 mg/kg, i.p., 30 h before reserpinization, or 10(-3) M in vitro) inhibited the reserpine-induced response, and zinc sulfate alone (10(-11)--10(-3) M) also stabilized lysosomal membrane permeability to beta-glucuronidase. No direct effect of zinc or reserpine on purified beta-glucuronidase activity was observed. In conclusion, it is postulated that the stabilizing effect of zinc on lysosomal membranes, as manifest by reduced release of beta-glucuronidase from isolated lysosomes, is one of the protective mechanisms of zinc against reserpine-induced ulceration.

Animals↗
PubMed1980

Studies of zinc and histamine on lysosomal fragility: possible role in stress ulceration.

A combined in vivo and in vitro study was undertaken with rats to test the hypothesis that zinc would protect against cold water immersion--restraint gastric ulcers, and that this phenomenon was mediated in part by stabilization of lysosomal membranes. This postulate was confirmed by observed activity changes in released beta-glucuronidase in mucosal tissue, as well as by dose-response in vitro data on isolated hepatic lysosomes exposed to zinc. Histamine, a known ulcer-enhancing agent, induced the opposite effect and increased the lysosomal release of this marker acid hydrolase.

Animals↗
PubMed1980

Inhibition by zinc of hepatic lysosomal release of beta-glucuronidase induced by phorbol-12-myristate-13-acetate (PMA).

The tumor promoter, phorbol-12-myristate-13-acetate (PMA), elicited a significant increase in lysosomal membrane permeability, as measured by release of free beta-glucurnidase, in guinea pig and hamster isolated hepatic lysosomes in vitro. This response was antagonized by zinc sulfate; zinc compounds having previously been shown to inhibit tumor growth at multiple sites in several species. Since phorbol ester tumor promotion is likely associated in part with actions on cellular membrane systems, its inhibition by zinc may relate to the membrane stabilizing activity of zinc compounds.

Animals↗
PubMed1980

Modulating effect by zinc on hepatic lysosomal fragility induced by surface-active agents.

In vitro studies on rat hepatic lysosomal stability, as assessed by release of beta-glucuronidase, were undertaken to demonstrate the comparative influence of surface-active agents which act by various mechanisms. Bile acids, short chain alcohols, acetylsalicylic acid, and Triton X-100 were studied, as well as their interaction with zinc. The detergents and alcohols enhanced release of this acid hydrolase in a dose dependent fashion, but acetylsalicylic acid did not. Zinc antagonized these effects in a non-specific manner. It is postulated that zinc stabilized lysosomes by direct action on the lysosomal membrane, such as by surface protein interactions, but the precise mechanism remains unknown.

Alcohols↗
PubMed1979

Cholinergic-mediated gastric mast cell degranulation with subsequent histamine H1-and H2-receptor activation in stress ulceration in rats.

The effects of atropine, mepyramine, metiamide or NaHCO3 on gastric ulceration, gastric secretion and gastric mast cell degranulation were studied in stressed pylorus-occluded rats. The influence of dexamethasone pretreatment on stress ulcers in animals without pylorus occlusion (intact rats) was also examined. Stress produced a high glandular lesion incidence and ulcer index, and markedly lowered gastric secretion and glandular wall mast cell counts. Injected 0.5 h before stress, atropine, mepyramine or metiamide strongly antagonised ulceration. Atropine or metiamide, but not mepyramine, reduced gastric secretion. Only atropine prevented stress-induced mast cell changes. NaHCO3, given intragastrically before stress, did not prevent ulceration or mast cell degranulation despite complete neutralisation of gastric acid. Dexamethasone-induced gastric mucosal mast cell depletion could reduce stress ulceration. The findings show that stress degranulates stomach mast cells via a cholinergic pathway; released histamine from this source is largely responsbile for gastric ulceration through H1- and H2-receptor effects. Histamine H2-receptor-mediated gastric acid may play only a small contributory role in stress ulcers in rats. The antiulcer mechanisms of histamine H1- and H2-receptor blockade are discussed.

Animals↗
PubMed1978

Some observations on the gastric effects of phentolamine in rats.

The effects of graded doses of phentolamine on gastric secretion, gastric emptying rate, gastric mucosal mucus content and gastric mucosal lesion incidence were studied in conscious rats 2 h after intramuscular administration. In pylorus-occluded rats, phentolamine (5, 10 or 20 mg/kg) produced dose-dependent decreases in the gastric secretory volume and total acid output. Similar doses of the drug also produced dose-dependent decreases in the gastric emptying rate in animals without pylorus occlusion (intact rats), but did not affect the gastric mucosal mucus content. The incidence of gastric mucosal lesions in pylorus-occluded or intact animals rose with increasing doses. The findings are discussed in the light of the possibility that phentolamine, in the dose range examined, possesses a sympathomimetic action which would underlie the gastric lesions observed.

Animals↗
PubMed1978

A correlative study of the antiulcer effects of zinc sulphate in stressed rats.

The effects on zinc sulphate pretreatment of rats on stress-induced gastric ulcers and on changes in mast cell counts were studied and correlated with changes in gastric mucosal microcirculation. The effects on zinc sulphate on blood pressure responses and on growth were also examined. Stress (2 h restraint at 4 degrees C) produced marked glandular mucosal ulceration, lowered the stomach wall mast cell counts and increased the microcirculatory blood volume in the superficial glandular mucosa. Zinc sulphate (22, 44 or 88 mg/kg; injected i.p. 48 h before stress) reversed all these changes in a dose-related manner. Blood pressure responses to i.v. acetylcholine, adrenaline or histamine were unaffected and growth of the rats as observed for 7 days after injection was not impaired. On the basis of these findings the mechanism of the antiulcer action of zinc sulphate is the following: inhibition of the stress-induced release of vasoactive agents from gastric mast cells and thus prevention of the subsequent microciculatory changes known to produce mucosal ulceration. Interference with vascular responses through direct blockade or toxicity is unlikely.

Animals↗