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Biomedical subjects

C H Cho

Publications and source records attributed to C H Cho.

At least 253 records · Page 14Linked to original sources
PubMed1978

Effects of zinc sulphate pretreatment on gastric acid secretion and lesion formation in rats infused intravenously with graded doses of methacholine.

The effects of intraperitoneal pretreatment with zinc sulphate (22, 44 or 88 mg/kg) were studied on gastric acid secretion and lesion formation induced by methacholine (125, 250 or 500 microgram/kg/h) infused intravenously in rats with stomachs perfused in situ. Graded infusions of methacholine produced dose-dependent increases in gastric acid secretion and lesion incidence in saline-pretreated control rats. These effects were progressively reduced by increasing pretreatment doses of zinc sulphate. The relationship between these findings and the action of zinc on gastric mast cells is discussed.

Animals↗
PubMed1978

Protection by zinc sulphate against reserpine-induced ulceration and other gastric effects in the rat.

The effects of intraperitoneal pretreatment, 48 h beforehand, with zinc sulphate (22, 44 or 88 mg/kg) were studied on gastric ulceration, gastric secretion and changes in stomach wall mast cell counts induced after 4 h by reserpine (5 mg/kg) given intraperitoneally to intact (unoperated for pylorus occlusion) or pylorus-occluded rats. Zinc sulphate dose-dependently antagonised the gastric actions of reserpine by preventing ulceration in the ruminal and glandular segments of the stomach, reducing acid secretion, and inhibiting mast cell degranulation which occurred mainly in the glandular mucosal layer. The relationship between these findings and the action of zinc on gastric mast cell is discussed.

Animals↗
PubMed1977

The effects of zinc sulphate on vagal-induced mast cell changes and ulcers in the rat stomach.

The effects of zinc sulphate pretreatment on the formation of gastric ulcers, changes in intragastric pressure and changes in the gastric mucosal mast cell count induced by electrical vagal stimulation were studied in anaesthetized rats. Vagal stimulation produced a high gastric glandular ulcer incidence and ulcer index, increased the intragastric pressure, and reduced the number of granulated mast cells in the gastric mucosa and submucosa. Pretreatment with zinc sulphate (22, 44 ot 88 mg/kg), injected i.p. 48 h beforehand, reversed the changes in these parameters in a dose-related manner. These observations suggest that the inhibitory effects of zinc sulphate on mucosal mast cell degranulation may account for its ability to antagonise vagal-induced gastric glandular ulceration. The mechanisms involved in the aetiology of this type of gastric ulcer are discussed in the light of these results.

Animals↗
PubMed1977

The effect of zinc on anaphylaxis in vivo in the guinea-pig.

The protective effects of pretreatment with zinc sulphate aerosols against bronchoconstriction induced by egg albumen or histamine aerosols were assessed in sensitized or non-sensitized guinea-pigs respectively. Pretreatment with an adequate concentration of zinc sulphate aerosol significantly prolonged the time of onset of bronchoconstriction in sensitized guinea-pigs challenged with egg albumen, but did not appreciably alter the onset time of histamine-induced bronchoconstriction in non-sensitized animals. These findings suggest that zinc aerosols may be of prophylactic value against bronchoconstriction of allergic origin.

Aerosols↗
PubMed1977

The hemostatic effects of orally administered Yunnan Bai Yao in rats and rabbits.

The effects of orally administered Yunnan Bai Yao were studied on the bleeding time in rats and the blood clotting time in rabbits. Significant decreases were seen in both the bleeding and clotting times, observed over a 4 h period following administration. These effects were seen as early as 1/2 h and were still present at 4 h. Graded doses of Yunnan Bai Yao produced dose-related decreases in blood clotting times in the rabbits. The findings suggest that some active principle, able to affect the hemostatic mechanism, is absorbed after oral administration of the herbal preparation.

Administration, Oral↗
PubMed1976

Intragastric NaHCO3 perfusion and vagal-induced ulcer formation in the rat stomach.

The effects of electrical vagal stimulation on gastric acid output and ulcer formation were studied in rats intragastrically perfused with saline or NaHCO3 solutions. Vagal stimulation produced a 100% incidence of glandular lesions and a significant increase in total acid output in saline-perfused stomachs. Antacid perfusion failed to prevent ulcer formation despite complete neutralization of the increased acid output. It is considered that vagal-induced gastric glandular lesions are not acid dependent.

Animals↗
PubMed1976

Acute gastric ulcer formation in response to electrical vagal stimulation in rats.

Intermittent electrical stimulation of the left cervical vagus increased intragastric pressure and induced a 100% incidence of haemorrhagic ulcers in the glandular mucosa of rat stomachs. Atropine pretreatment of sub-diaphragmatic vagotomy prevented these effects. The findings substantiate the idea that stress-induced glandular ulcers result from vagal-mediated increased gastric contractions.

Animals↗
PubMed1976

Effects of zinc chloride on gastric secretion and ulcer formation in pylorus-occluded rats.

The effects of 10-day pretreatment with i.p. injections of zinc chloride, 16 mg/kg, on gastric secretion and on gastric ulceration induced by stress or by acid accumulation were examined in pylorus-occluded rats. Zinc chloride pretreatment significantly reduced the volume of gastric secretion and the total acid output as well as the incidence of gastric ulcers induced either by stress or by acid accumulation. The findings support the idea zinc compounds may be useful in the treatment of gastric ulcers.

Animals↗
PubMedDate not supplied

Role of opioid receptors in cardioprotection of cold-restraint stress and morphine.

Since cold exposure confers cardioprotection, the present study attempted to determine the role of opioid receptors (OR). Stress with cold exposure and restraint for 3 h, shown previously to induce peptic ulcer in a synergistic manner, attenuated infarct size induced by myocardial ischemia and reperfusion in the isolated perfused rat heart from 36.64 +/- 1.8 to 22.85 +/- 2.6%. This is similar to protecting the rat with morphine at 8 mg/kg, which also attenuated the infarct size from 36.26 +/- 1.6 to 20.30 +/- 2.1%. The effects of cold-restraint or morphine were abolished by naloxone, a non-selective OR antagonist; nor-binaltorphimine, a selective kappa-OR antagonist; naltrindole, a selective delta-OR antagonist, or CTOP, a selective mu-OR antagonist. The effects were also attenuated by blockade of protein kinase C or the mitochondrial K(ATP) channel. The finding is first evidence that all three OR subtypes mediate cardioprotection of cold-restraint stress in the rat.

Adenosine Triphosphate↗
PubMedDate not supplied

Current roles of nitric oxide in gastrointestinal disorders.

It has been confusing as to what roles nitric oxide (NO) has in different physiological and pathological mechanisms in various diseases. In the gastrointestinal tract, NO can be either protective or deleterious in different disorders. This depends on what type of nitric oxide synthase (NOS) is involved in these pathological conditions. Constitutive NOS (cNOS) is responsible for production of NO in physiological context. In contrast, inducible NOS (iNOS) produces NO in pathophysiological circumstances. NO is implicated in mechanisms maintaining the integrity of the gastric epithelium. In this connection, it regulates gastric blood flow and directly stimulates gastric mucus secretion by activating soluble guanylate cyclase. A blockade of NO production resulted in an impairment of the vascular response and the subsequent alkaline flux in the lumen. This would impair the restitution process. Endogenous NO also contributes to the inhibition of acid secretion in the stomach. Indeed the adverse action of cigarette smoking on ulcer healing is largely dependent on the deficiency of cNOS and a subsequent depression of gastric blood flow and angiogenesis. To this end, NO may act as a crucial signal to promote endothelial cell differentiation into vascular tubes. In experimental colitis, NO derived from iNOS, together with other free radicals contribute significantly to the inflammatory response in the colon. It is also involved in the ulcerogenic effect of passive smoking on colitis. The mechanism is likely mediated through the interaction with superoxide to produce peroxynitrite, a strong oxidizing agent that initiates lipid peroxidation. In conclusion, NO in low concentration derived from cNOS is cytoprotective by directly acting as an inducer of defense responses in the gastrointestinal tract. However, higher concentrations of NO from iNOS exhibit toxic effects through nitrosative and oxidative stress.

Animals↗
PubMedDate not supplied

Dissociation between the renal and blood acid-base actions of acetazolamide in restraint-stressed rats.

Subcutaneous injection of acetazolamide (50 or 200 mg/kg) markedly increased the blood H+ and lowered the HCO3- concentrations in a dose-related manner. The urinary pH and HCO3- excretion were elevated. Restraint stress normalized the blood HCO3- levels but not the H+ concentrations; the high levels of urinary pH and the HCO3- content were unaffected in the acetazolamide-treated animals. These findings suggest that acetazolamide induces metabolic acidosis which appears not to be caused by depletion of blood HCO3- through increased urinary HCO3- excretion. Instead, an extra-renal mechanism could be responsible for the increased blood H+ concentration. Restraint stress significantly decreased the respiratory rate, which was prevented by acetazolamide pretreatment. The reversal of restraint-stress-induced respiratory depression by acetazolamide is probably due to the activation of both peripheral and medullary chemoreceptor sites by acidosis.

Acetazolamide↗
PubMedDate not supplied

Effects of long-acting somatostatin analogue (Sandostatin) on manifest diabetic ketoacidosis.

Insulin deficiency and counterregulatory hormone excess are the basic process in the development of diabetic ketoacidosis (DKA). Somatostatin, which suppresses the secretion of glucagon and growth hormone, has been known to attenuate the rate of gluconeogesis and ketogenesis in insulin-dependent diabetes mellitus patients. However, the therapeutic efficacy of somatostatin has not been approved to be practical in the treatment of manifest DKA. To examine the additive effect of octreotide, the synthetic long-acting somatostatin analogue SMS 201-995, to conventional treatment of manifest DKA, we compared the correction time of acidosis, ketonuria, and hyperglycemia of patients treated with an intravenous infusion of low-dose insulin (4 units per hour) plus subcutaneous injection of octreotide (50 microg every 6 hours) by low-dose insulin alone. The correction time for hyperglycemia and acidosis did not show any difference between groups (p = 0.089, p = 0.82). However, the time for disappearance of ketonuria of the octreotide-treated group (38.0 +/- 32.0 h) was reduced significantly compared to other group (68.3 +/- 26.0 h) (p = 0.048). These results indicated that the addition of octreotide to conventional treatment of DKA might improve the correction of ketosis, but would not allow more rapid control of acidosis and hyperglycemia in manifest DKA.

Adolescent↗