Biomedical subjects

C H Cho

Publications and source records attributed to C H Cho.

At least 109 records · Page 6Linked to original sources

PubMed1997

Tungstic acid reduction of cold-resistant stress-induced ulceration in rats.

Sprague-Dawley rats were restrained at 4 degrees C for 2 h (stress). Tungstic acid in a single dose of 0.01, 0.1, 1, 10, 100 or 300 mg/kg (dissolved in distilled water) was administered intragastrically to animals 30 min prior to stress. Stress induced significant gastric mucosal damage, whereas tungstic acid pretreatment dose-dependently reduced lesion formation. Doses of tungstic acid of 1 mg/kg and higher significantly (P < 0.05-0.001) decreased ulcers. The mucosal mast cell counts in rats pretreated with tungstic acid were significantly higher than those of control rats. In motility experiments using oral administration of amberlite pellets, pretreatment with tungstic acid dose-dependently reduced the gastric emptying rate during a 1 h period of stress. Gastric mucosal xanthine oxidase and superoxide dismutase (SOD) activities, after pretreatment with a single dose of tungstic acid, were not altered in stressed animals. It is suggested that tungstic acid effectively antagonizes stress-induced gastric ulcers, possibly by decreasing motility and mass cell degranulation. Xanthine oxidase and SOD activities and mucous content were not changed in the gastric mucosa by the present method of tungstic acid administration.

Animals↗

PubMed1997

Effects of selective beta-adrenoceptor antagonists on gastric ulceration in the rat.

Metoprolol and butoxamine, beta-adrenoceptor antagonists which act selectively at the beta 1- and beta 2-adrenoceptors, respectively, have been investigated for their actions on the ethanol, indomethacin and cold-restraint stress ulcer models. Oral administration of butoxamine but not metoprolol significantly attenuated gastric mucosal damage in the three types of ulcer model. Intraperitoneal injection of butoxamine reduced indomethacin ulceration but not that of the other two models. The stimulatory effect of butoxamine on the gastric mucosal potential difference and intramucosal mucus level correlated positively with its anti-ulcer action. Only oral administration of butoxamine significantly increased the mucosal prostaglandin E2 (PGE2) level but not after intraperitoneal injection. Oral administration of butoxamine also significantly increased the mucosal PGE2 level in the three types of ulcer model but this drug was only effective in the indomethacin ulcer model after intraperitoneal injection. Gastric acid and pepsin output were not affected by either drug. Metoprolol significantly reduced systemic blood pressure; this could be attributed to a reduction in gastric mucosal blood flow. These results imply that beta 2-adrenoceptors play a significant role in the pathogenesis of gastric ulceration. We suggest that the anti-ulcer effect of butoxamine was in part a result of strengthening of the mucosal barrier but that this was not effected by modification of acid or pepsin secretions in the stomach. Stimulation of PGE2 in the gastric mucosa could contribute in part to the anti-ulcer action of the drug, especially when given by the oral route.

Adrenergic beta-Antagonists↗

PubMed1997

Regional vascular mechanical properties by 3-D intravascular ultrasound with finite-element analysis.

A method employing intravascular ultrasound (IVUS) and simultaneous hemodynamic measurements, with resultant finite element analysis (FEA) of accurate three-dimensional IVUS reconstructions (3-DR), was developed to estimate the regional distribution of arterial elasticity. Human peripheral arterial specimens (iliac and femoral, n = 7) were collected postmortem and perfused at three static transmural pressures: 80, 120, and 160 mmHg. At each pressure, IVUS data were collected at 2.0-mm increments through a 20.0-mm segment and used to create an accurate 3-DR. Mechanical properties were determined over normotensive and hypertensive ranges. An FEA and optimization procedure was implemented in which the elemental elastic modulus was scaled to minimize the displacement error between the computer-predicted and actual deformations. The "optimized" elastic modulus (Eopt) represents an estimate of the component element material stiffness. A dimensionless variable (beta), quantifying structural stiffness, was computed. Eopt of nodiseased tissue regions (n = 80) was greater than atherosclerotic regions (n = 88) for both normotensive (Norm) and hypertensive (Hyp) pressurization: Norm, 9.3 +/- 0.98 vs. 3.5 +/- 0.30; Hyp, 11.3 +/- 0.72 vs. 8.5 +/- 0.47, respectively (mean +/- SE x 10(6) dyn/cm2; P < 0.01 vs. nondiseased). No differences in beta between nondiseased and atherosclerotic tissue were noted at Norm pressurization. With Hyp pressurization, beta of atherosclerotic regions were greater than nondiseased regions: 21.5 +/- 2.21 vs. 14.0 +/- 2.11, respectively (P < 0.03). This method provides a means to identify regional in vivo variations in mechanical properties of arterial tissue.

Arteriosclerosis↗

PubMed1997

Ureteral fibroepithelial polyp associated with ureteropelvic junction obstruction in a child.

Ureteral fibroepithelial polyp is an unusual benign tumor of a mesodermal origin. It is very rare in infants and children, and the majority of them, excluding ones secondary to chronic irritation, were presented as a single disease without associated lesion. We report a case of multiple ureteral fibroepithelial polyps associated with ureteropelvic junction obstruction in a 5 year-old boy.

Child, Preschool↗

PubMed1997

Electron microscopic perspectives of gill pathology induced by 1-naphthyl-N-methylcarbamate in the goldfish (Carassius auratus Linnaeus).

This experiment has clarified the ultrastructural pathology, by scanning (SEM) and transmission electron microscopy (TEM), induced by 1-naphthyl-N- methylcarbamate (carbaryl) in the gills of juvenile goldfish (Carassius auratus Linneaus). Carbaryl is a low toxicity pesticide commonly used in forestry and agriculture and for controlling aquatic weeds and crustacean predators of shellfish, and has been known to cause gill damage in fish and clams. A variety of cellular changes were observed after exposure of goldfish for 96 h to a sublethal dose of 10 mg carbaryl/l of water. SEM revealed secondary lamellar fusion, distortion, thinning, and mucus release. TEM responses included enlargement of subepithelial lymphatic spaces and mitochondrial disruption and distortion of the lamellar covering epithelium. Pillar cells became detached and chloride cells were vacuolated. Fish were able to withstand these changes in subacute experiments due to redundancy in gill surface area.

Animals↗

PubMed1996

A mechanistic study of beta-adrenoceptor antagonists on ethanol-induced gastric damage.

The beta-adrenoceptor subtypes and the roles of myeloperoxidase and prostaglandin E2 in the anti-ulcer effect of beta-adrenoceptor antagonists were studied. A non-selective beta-adrenoceptor antagonist, propranolol, or selective beta-adrenoceptor antagonists, metoprolol (a beta 1-adrenoceptor antagonist) or butoxamine (a beta 2-adrenoceptor antagonist) were used. Propranolol given either intraperitoneally or orally reduced ethanol-induced mucosal damage and myeloperoxidase activity. Oral administration of butoxamine produced similar effects. The blood neutrophil count was increased after ethanol administration and this was reversed by the two drugs. Metoprolol did not affect myeloperoxidase activity, neutrophil count and mucosal damage under these experimental conditions. Oral administration of propranolol or butoxamine increased mucosal prostaglandin E2 level. It is concluded that the inflammatory responses to ethanol, as indicated by neutrophil infiltration in gastric mucosa, can be specifically inhibited by drugs that block beta 2-adrenoceptors. This action would explain in part why propranolol and butoxamine but not metoprolol lessened gastric damage. In addition, oral administration of propranolol and butoxamine increased the mucosal prostaglandin E2 level, which could partially contribute to their anti-ulcer effects.

Adrenergic beta-Antagonists↗

PubMed1996

An experimental model for studying passive cigarette smoking effects on gastric ulceration.

Cigarette smoking is associated with gastric mucosal damage in humans. For this study, a smoke chamber was designed to investigate the effects of passive smoking on gastric ulceration. Different concentrations of cigarette smoke (0%, 1%, 2%, and 4%) were perfused into a chamber for one hr in which conscious rats were placed. This one-hr smoke exposure potentiated ethanol (70%, v/v, p.o.)-induced gastric mucosal damage and increased serum nicotine levels; however, it did not affect the blood pH, pCO2, pO2, and HCO3 concentrations, or the systemic blood pressure and heart rate. Under these experimental conditions, exposure to cigarette smoke produced no significant changes in the blood acid/base balance and stress in the animals but significantly potentiated ethanol-induced gastric mucosal damage. The present experimental model is suitable for studying the adverse interactions between passive smoking and alcohol drinking in gastric ulcer formation in rats.

Animals↗

PubMed1996

A study of the antiulcer mechanisms of propranolol in rats.

Although propranolol has been shown to protect against ethanol and stress ulceration, the antiulcer mechanisms are still unclear. The present study examined the antiulcer mechanisms of propranolol in three different types of ulceration induced respectively by ethanol (60%), indomethacin (30 mg/kg) and stress (cold-restraint). Propranolol pretreatment in the highest dose (10 mg/kg) given either intraperitoneally (i.p.) or orally (p.o.) prevented gastric mucosal damage in these three ulcer models. The three doses of the drug (2.5, 5 or 10 mg/kg) dose-dependently decreased systemic blood pressure which was accompanied by a reduction of gastric mucosal blood flow. These findings suggest that the protection was unrelated to an improvement of local circulation in the stomach. However, propranolol preserved the mucus levels in the three types of ulcer models. The beta-adrenoceptor blocker also increased the basal gastric mucosal potential difference. These findings indicate that propranolol strengthens the mucosal barrier by the preservation of mucosal mucus and enhancement of the mucosal integrity in the stomach.

Adrenergic beta-Antagonists↗

PubMed1996

Liquid water and biological systems: the most important problem in science that hardly anyone wants to see solved.

The main emphasis of this paper is the design of a water model that gives the correct temperature-dependent density. Water interaction models currently used have been highly oversimplified and are presently incapable of producing, over even a modest range of temperature and pressure, the properties of real water. The new feature is a modified second-neighbour non-hydrogen-bonded interaction to match those known to exist in the moderately dense ice polymorphs or the high density amorphous solid. Combined dynamically in the liquid with ordinary tetrahedral bonding, the more dense metastable structure tends to grow in with increasing temperature because of the entropic driving force, creating the density maximum. With this new model, more realistic structural and dynamic properties of liquid water near surfaces, particularly biologically important macromolecules and membranes, can be expected in future work.

Animals↗

PubMed1996

Vagal hyperactivity in stress induced gastric ulceration in rats.

Indirect evidence suggests that stress ulceration is provoked by vagal hyperactivity. However, direct evidence of hypervagal activity during stress conditions is lacking. Experiments were designed to directly measure vagal activity under different stress conditions in rats. Starvation stress for 48 h did not change the mean amplitude of action potentials, but their frequency was significantly decreased. Restraint stress at 22 degrees C increased vagal activity, both amplitude and frequency, in the first 60 min; these responses were markedly enhanced by cold (4 degrees C) and persisted for at least 2 h. Starvation for 48 h did not induce any gastric mucosal lesions. Restraint alone produced petechiae in the gastric mucosa, but cold restraint induced severe haemorrhagic ulcers. It is concluded that cold restraint stress provokes a prolonged vagal hyperactivity, which is one of the causative factors for gastric ulceration.

Animals↗

PubMed1996

Adaptive gastric mucosal cytoprotection in rats: different modes of action by three mild irritants.

The mechanisms of adaptive mucosal cytoprotection by mild irritants were investigated in rats. In an ex vivo chamber preparation, application of 20% ethanol, 5% NaCl or 0.3 M HCl to the posterior side of the mucosa significantly protected that side of the stomach against mucosal damage caused by subsequent exposure to 100% ethanol, with contralateral transmission of protection to the anterior side by 20% ethanol and 0.3 M HCl. Atropine or lidocaine significantly reversed the cytoprotection of 20% ethanol. Bilateral vagotomy partially prevented the antilesion action of 20% ethanol, and completely prevented the action of 0.3 M HCl. However, the three mild irritants did not affect gastric mucosal blood flow, but restored the ion transport mechanism which was depressed by ethanol. It is therefore concluded that the three mild irritants have their own distinctive cytoprotective mechanisms against ethanol ulceration, which is predominantly not mediated by effects on the vascular system of the gastric mucosa.

Animals↗

PubMed1996

Effects of chronic nitric oxide synthase inhibition in cold-restraint and ethanol-induced gastric mucosal damage in rats.

Gastric actions of Nw-nitro-1-arginine methyl ester (L-NAME) were investigated in rats, as this agent is a reliable nitric oxide synthase inhibitor L-NAME solutions were placed in subcutaneous osmotic minipumps which continuously released L-NAME at 0.1, 1.0, 10, or 40 mg/kg/day. L-NAME dose and time-dependently enhanced stress-induced gastric ulceration but did not affect mucosal mast cell population. Ulcerogenic actions of L-NAME were reversed by L-arginine but not by D-arginine. Ten L-NAME treatment also enhanced the ethanol-induced gastric mucosal damage, depressed gastric mucosal blood flow but did not alter gastric mucus, secretory volume, or acid output. It is concluded that in the present models, chronic nitric oxide synthase inhibition enhanced ulcerogenesis by decreasing mucosal resistance due to reduced mucosal blood perfusion. This implicates nitric oxide as a mucosal defense factor which acts in part by maintaining mucosal blood flow.

Animals↗

PubMed1996

Transcatheter instillation of urokinase into loculated pleural effusion: analysis of treatment effect.

OBJECTIVE: Our objective was to evaluate the usefulness of intracavitary instillation of urokinase in the treatment of loculated pleural effusion. SUBJECTS AND METHODS: We analyzed CT and sonographic scans of 31 patients with loculated pleural effusion treated with intracavitary urokinase. When the drainage was less than 100 ml/day, urokinase was instilled through the catheter until the drainage was less than 50 ml/day. Response to the treatment was assessed on follow-up chest radiographs and classified into three groups: completely effective (lung expansion > 80%), partially effective (20-80%), and ineffective (< 20%). The sonographic pattern of pleural fluid was classified as anechoic, linear septated, or honeycomb, and the thickness of the parietal pleura was measured on CT scans. RESULTS: Of the 16 patients in whom treatment was completely effective, sonography showed an anechoic appearance in 12 and a linear septated appearance in four, and the thickness of the parietal pleura on CT scans was 2 mm in six, 3 mm in seven, and 4 mm in three. Of the nine patients in whom treatment was partially effective, sonography showed an anechoic appearance in six and a linear septated appearance in three, and the thickness of the parietal pleura on CT scans was 3 mm in five and 4 mm in four. Of the six patients in whom treatment was ineffective, sonography showed a linear septated appearance in one and a honeycomb appearance in five, and the thickness of the parietal pleura on CT scans was 3 mm in one, 4 mm in two, 5 mm in one, and 6 mm in two. CONCLUSION: Urokinase instillation through a percutaneous catheter was effective in the treatment of loculated pleural effusion in most patients but was not effective in patients whose pleural fluid had a honeycomb appearance on sonography or whose parietal pleura had a thickness of more than 5 mm on CT scans.

Adolescent↗

PubMed1996

The antilesion actions of anticholinergic agents on ethanol-induced injury in rat stomachs: the importance of gastric vascular integrity and tonicity.

1. The antilesion actions of two antimuscarinic drugs on ethanol-induced gastric injury and mucosal integrity were examined in male rats. Histological examinations were made and gastric emptying rates determined after in vivo administration of the drugs to conscious rats. In anaesthetized rats, with an ex vivo gastric chamber, effects on gastric transmucosal potential difference, Evan's blue leakage and Na+ output were examined. 2. In conscious animals, atropine (1 mgkg-1, i.p.) and pirenzepine (1 mgkg-1, i.p.) both significantly reduced macroscopic lesion formation, but not microscopic damage and functional alterations, caused by orally administered absolute ethanol. Moreover, these drugs did not show any effect on the basal gastric adherent mucus level, nor the depleting action of ethanol on both adherent mucus and the mucosal mucus layer. Nevertheless, both atropine and pirenzepine significantly reduced gastric emptying rate. 3. In anaesthetized animals, pirenzepine but not atropine increased the basal transmucosal potential difference (PD); however, it could not prevent the ethanol-induced drop in PD. Furthermore, the inhibitory action of ethanol on sodium ion output from the gastric mucosa was not attenuated by these drugs. Pirenzepine, however, significantly lessened the increase in vascular permeability caused by 100% ethanol. This action was not shared by atropine. 4. These findings indicate that both atropine and pirenzepine exert their antilesion actions through the relaxation of the stomach. Pirenzepine also preserves the integrity of the gastric mucosal vasculature, which is distinct from the action of atropine. The protective action of these drugs occurs only at the macroscopic level.

Animals↗

PubMed1995

Evidence for potential application of zinc as an antidote to acetaminophen-induced hepatotoxicity.

The therapeutic application of zinc sulphate as an antidote to acetaminophen overdose was examined in ICR mice. Hepatotoxicity was induced by a single oral dose of acetaminophen (750 mg/kg). Various treatments (normal saline, 15 or 30 mg/kg zinc sulphate, 150 mg/kg N-acetylcysteine, 15 mg/kg zinc sulphate + 150 mg/kg N-acetylcysteine) were given i.p. 1 h after acetaminophen overdose. Serum alanine aminotransferase, hepatic glutathione and malondialdehyde levels were measured before experiments and at various intervals after the administration of acetaminophen. Serum acetaminophen levels were also measured at different different intervals. Zinc sulphate showed protection by dose-dependently reducing alanine aminotransferase and malondialdehyde levels. The drug also partially prevented the depletion of hepatic glutathione. These effects were not as good as those of N-acetylcysteine. However, the combination of zinc sulphate with N-acetylcysteine produced even better protective effects. Furthermore, drug treatments did not affect serum acetaminophen levels. It is concluded that both drugs attenuate acetaminophen-induced hepatic toxicity, and the action is likely to be mediated through replenishment of hepatic glutathione levels. The use of zinc sulphate alone or in combination with N-acetylcysteine could be another alternative for the treatment of acetaminophen overdose in view of possible side effects produced by N-acetylcysteine.

Acetaminophen↗

PubMed1995

The importance of gastric emptying and mucosal folds in the adaptive cytoprotection of mild irritants in rats.

This study examines the involvement of gastric emptying and mucosal folds in the adaptive cytoprotection of different mild irritants against 100% ethanol-induced gastric mucosal damage. Pre-exposure to either 20% ethanol, 5% NaCl or 0.3M HCl significantly reduced the gastric mucosal damage caused by 100% ethanol in rats. Administration of either one of the three mild irritants increased the basal gastric residual volume and decreased the area occupied by gastric mucosal folds, but only 20% ethanol reduced the gastric emptying rate. Indomethacin (5 mg/kg, s.c.) pretreatment did not affect ethanol ulceration and gastric emptying rate when given by itself, but reversed the flattening of mucosal folds produced by the three mild irritants, and abolished the protective effect of 20% ethanol. These results suggest that the gastric adaptive cytoprotection induced by the three mild irritants acts through luminal dilution of the noxious agent, possibly caused by gastric retention. The reduction of mucosal folds could also contribute to the anti-lesion action of 20% ethanol. It is therefore suggested that the protective actions of the three mild irritants act through different mechanisms.

Adaptation, Physiological↗

PubMed1995

The role of non-protein sulfhydryl compounds in gastric adaptive cytoprotection against ethanol-induced mucosal damage in rats.

The contribution of the endogenous nonprotein sulfhydryl compounds (SH) in gastric adaptive cytoprotection was investigated in rats. N-ethylmaleimide (NEM) treatment significantly reduced mucosal SH level, and aggravated the mucosal injury induced by absolute ethanol. Oral administration of the mild irritants, 20% ethanol, 5% NaCl or 0.3 M HCl, significantly increased the basal mucosal SH level. These agents also showed a cytoprotective action against the necrotizing effect of absolute ethanol. Administration of NEM did not alleviate this cytoprotective potential, although it abolished the increased SH level evoked by these mild irritants. Thus, it is concluded that modulation of endogenous SH by mild irritants perhaps only plays a minor role in the gastric adaptive cytoprotection.

Administration, Oral↗

PubMed1995

Glutaric aciduria: improved MR appearance after aggressive therapy.

Advances in understanding the metabolic abnormalities which cause glutaric aciduria allow biochemical diagnosis on the basis of deficient enzyme and the potential for therapy. Brain abnormalities associated with this inborn error of metabolism have been demonstrated with CT and MR. The findings typically described are atrophy of the fronto-temporal regions with large insular cisterns and diffuse white matter hypodensities. We present a patient with glutaric aciduria, confirmed by enzymatic assay, who had these findings on CT and MR examination. Repeat imaging demonstrated significant improvement after dietary therapy and aggressive prevention of catabolism during febrile illness.

Amino Acid Metabolism, Inborn Errors↗