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Biomedical subjects

C H Cho

Publications and source records attributed to C H Cho.

At least 181 records · Page 10Linked to original sources
PubMed1990

The interaction of ethanol and zinc on hepatic glutathione and glutathione transferase activity in mice.

The effects of ethanol and/or zinc sulphate on liver glutathione and glutathione transferase activity were studied in mice. Ethanol suppressed glutathione transferase activity and had no significant effect on glutathione levels in the organ. Zinc sulphate administration dose-dependently increased glutathione transferase activity but did not affect hepatic glutathione content. Furthermore, the depressive action of ethanol on glutathione transferase activity was prevented by zinc sulphate pretreatment. It is suggested that zinc sulphate can reactivate glutathione transferase which in turn increases the excretion of the active metabolites produced by ethanol, through conjugation with glutathione in the liver. This action of zinc may alleviate the hepatic toxicity of ethanol in mice.

Animals↗
PubMed1990

Endogenous prostaglandins: its role in gastric mucosal blood flow and ethanol ulceration in rats.

The involvement of endogenous prostaglandins (PGs) in modulating gastric mucosal blood flow (GMBF) is still unclear. The present study was designed to demonstrate the role of this autacoid in the basal GMBF and the restoration of blood flow after restriction of blood supply to the stomach. The ex-vivo gastric chamber was prepared and the GMBF was measured by a laser Doppler technique. 20% ethanol incubation for 10 min in the chamber increased the basal GMBF and lessened the reduction of blood flow induced by absolute ethanol. It also decreased lesion formation caused by ethanol. Indomethacin 5 mg/kg, given s.c 60 min before experimentation had the opposite effects. Ligation of the gastric artery for 20 min which reduced the GMBF by 60%, worsened ethanol ulceration. There was a marked rebound of the GMBF after the ligation was released. Indomethacin totally abolished the blood flow rebound and aggravated ethanol ulceration. However, 20% ethanol incubation significantly potentiated such a rebound in blood flow and reduced lesion formation. Indomethacin pretreatment reversed these actions, whereas misoprostol administration produced the similar effects as 20% ethanol. It is concluded that GMBF plays an important role in ethanol ulceration and both basal and rebound GMBF is probably modulated by endogenous PGs.

Alprostadil↗
PubMed1990

Paracetamol potentiates stress-induced gastric ulceration in rats.

The effect of paracetamol on gastric ulcers produced by restraint at 4 degrees C for 2 h (stress) was studied in rats. Paracetamol treatment s.c. or p.o., with a dose as high as 250 mg kg-1, did not produce any haemorrhagic lesions in the glandular mucosa. Oral administration with 250 mg kg-1, however, significantly reduced the mast cell count in the gastric glandular mucosa and potentiated haemorrhagic ulceration but not mast cell degranulation caused by stress. The potentiating action was maximum when paracetamol was given between 15 and 30 min before stress. Ranitidine, astemizole, dimethylsulphoxide, sucralfate and verapamil did not protect against the adverse action of paracetamol on stress-evoked lesions. This study suggests that paracetamol worsens stress-induced stomach ulceration by an action which appears not to be due to histamine release, free radical production or intracellular calcium disturbance in the gastric mucosa.

Acetaminophen↗
PubMed1990

Inhibition of stress-induced gastric ulcers by sulphasalazine and its constituents (sulphapyridine and 5-aminosalicylic acid) in rats.

The effects of sulphasalazine and of its major constituents, sulphapyridine and 5-aminosalicylic acid (5-ASA), on gastric ulceration as well as on changes in mast cell counts and mucus levels in the glandular mucosa were examined in restrained rats exposed to 4 degrees C (stress) for 2 h. Sulphasalazine (50, 100, 200 mg/kg), sulphapyridine (31.25, 62.5, 125 mg/kg) or 5-ASA (18.75, 37.5, 75 mg/kg) was injected subcutaneously 0.5 h before stress induction. Cold-restraint stress produced gastric glandular mucosal ulcers which were significantly reduced by all three doses of sulphasalazine and the higher doses of sulphapyridine and 5-ASA. Sulphasalazine prevented mast cell degranulation and increased the amount of mucus adhering to the mucosa. In contrast, the higher doses of sulphapyridine significantly increased only the mucus levels, whereas those of 5-ASA effectively prevented mast cell degranulation. The results show that the total effect of sulphasalazine is approximately equivalent to the summation of the actions of its component doses of sulphapyridine and 5-ASA. It is notable that sulphapyridine itself appears to be biologically active in reducing ulcer severity.

Aminosalicylic Acids↗
PubMed1990

The role of serotonin in ethanol-induced gastric glandular damage in rats.

The effects of serotonin (5-HT) or methysergide (a 5-HT antagonist), given intraperitoneally 30 min beforehand, on ethanol-induced mucosal injury and mucosal blood flow were studied in rats. 5-HT itself dose dependently decreased the gastric mucosal mucus content and induced gastric damage in conscious animals. It also worsened ethanol-induced lesion formation but not mucus depletion. Methysergide pretreatment only prevented the former action. In the ex vivo chamber preparation, 5-HT lowered the gastric mucosal blood flow and produced mucosal damage in unconscious animals. It also potentiated ethanol-induced gastric injury and 5-HT release. Methysergide significantly prevented lesion formation and 5-HT release in ethanol-treated rats. Ethanol decreased the gastric mucosal blood flow in the mucosa which had been preincubated with HCl. This depression of gastric mucosal blood flow was further reduced by 5-HT, but was reversed by methysergide. The lesion-potentiating or -protecting actions of 5-HT or methysergide, respectively, suggest that the amine is involved in gastric mucosal damage by ethanol in rats.

Animals↗
PubMed1990

Observations on cardiac ultrastructure of the adult Japanese newt, Cynops pyrrhogaster.

Investigation of atrial and ventricular cardiac ultrastructure by transmission and scanning electron microscopy of the adult Japanese newt, Cynops pyrrhogaster, has revealed some unique cell types and features in this amphibian. Typical urodelan-type thin trabeculae composed of myocytes with conventional architecture of loosely scattered myofibrils were observed. Scarce granules of variable size and density were seen in atrial myocytes, and some Purkinje-like fibers were observed. Unique structures included scattered endocrine-like cells with dense cytoplasmic granules in the epicardial spaces, a distinct granular cell found occasionally on the endocardial surface projecting into the lumen of the cardiac trabeculae, and peculiar granulated inclusions in the myoplasm. The function of these possible endocrine cells remains undetermined. It is important to characterize the heart of this species, as it has recently been proven to be an excellent model for prolonged experimental studies in vitro.

Animals↗
PubMed1989

The protective mechanism of FPL55712 against stress-induced gastric ulceration in rats.

Cold-restraint stress produced stomach ulceration which was accompanied by a decreased glandular mucosal mast cell count and blood flow. Pretreatment with FPL55712, a leukotriene antagonist, dose-dependently prevented ulcer formation and mast cell depletion; however, it did not affect the reduced mucosal blood flow, nor did it significantly influence acid secretion and pepsin output. The role of the leukotrienes in stress ulceration is discussed in the light of the findings with FPL55712 on gastric glandular mucosal mast cell degranulation.

Animals↗
PubMed1989

Effects of zinc and cholesterol/choleate on serum lipoproteins and the liver in rats.

The effects of short-term treatment with orally-administered zinc sulphate and/or a mixture of cholesterol/choleate on serum lipoprotein and hepatic enzyme levels were studied. Administration of graded doses of zinc sulphate (20 or 40 mg/kg, as zinc ion) for 5 days, dose-dependently increased serum and hepatic zinc levels but depressed the serum high-density lipoprotein-cholesterol (HDL-C) concentration and liver cytochrome P-450 activity. However, it did not affect hepatic concentrations of malondialdehyde and free beta-glucuronidase. Cholesterol/choleate treatment for 5 days markedly damaged the liver, as reflected by elevations of hepatic concentrations of malondialdehyde (both in the mitochondrial and microsomal fractions) and of free beta-glucuronidase; total cholesterol and low-density lipoprotein-cholesterol in the blood were increased, whereas HDL-C was decreased significantly. Concomitant administration of zinc sulphate with cholesterol/choleate further lowered HDL-C levels, but reversed the high hepatic concentrations of both malondialdehyde and free beta-glucuronidase. The present study indicates that both zinc ions and cholesterol can decrease circulatory HDL-C levels and that zinc protects against cholesterol-induced hepatic damage by reducing lysosomal enzyme release and preventing lipid peroxidation in the liver.

Animals↗
PubMed1989

The antiulcer effect of verapamil in relation to gastric calcium levels in stressed rats.

The antiulcer effect of verapamil, and its relationship to stomach calcium levels, were examined in rats restrained at 4 degrees C (stress). Stress for 2 hr significantly increased muscle calcium and induced mucosal ulceration in the gastric glandular segment; calcium concentrations in the glandular mucosa and serum were unaffected. Verapamil or calcium gluconate given 30 min before stress prevented the rise in gastric muscle calcium, and attenuated ulcer severity. Bis(beta-aminoethylether)-NNN'N'-tetra-acetic acid (EGTA) pretreatment, however, further elevated stomach muscle calcium and markedly worsened lesion formation. These findings suggest that increased stomach muscle calcium could be a causal factor in stress-induced gastric glandular ulceration.

Animals↗
PubMed1989

Does acidosis contribute to stress-induced ulceration in rat stomachs?

The present study examines the involvement of acidosis in stress ulceration in rat stomachs. Cold restraint stress for 2 hr did not affect the blood lactate level; however, it produced respiratory acidosis, as reflected by the depressed respiratory rate which was associated with increased CO2 tension and a lowered blood pH. Severe hemorrhagic ulceration was found in the glandular mucosa. The effects of stress on blood pH and the stomach were reversed by IV infusion of NaHCO3. Infusion of HCl IV decreased the blood pH and HCO-3 level and produced gastric ulceration. It is concluded that respiratory acidosis could be involved in stress ulceration. The metabolic acidosis evoked by HCl also induced gastric damage, but the effect was much less.

Acidosis, Respiratory↗
PubMed1989

Modulating action of melatonin on serotonin-induced aggravation of ethanol ulceration and changes of mucosal blood flow in rat stomachs.

Effects of melatonin and serotonin on ethanol ulceration and mucosal blood flow in the rat stomach were investigated. Melatonin and serotonin (5-HT) administration did not produce observable gastric injury in the ex vivo stomach, but the 5-HT dose dependently reduced glandular mucosal blood flow (GMBF) in this organ. Ethanol depressed GMBF and induced visible glandular mucosal injury. The latter effect was prevented by melatonin preincubation. Serotonin pretreatment aggravated the gastric mucosal injury and GMBF changes induced by ethanol; these actions were partially reversed by melatonin. The findings indicate that the GMBF and gastric injury are related; the reduction in FMBF, however, may not be the sole factor responsible for ulceration. The antagonistic effects of melatonin on 5-HT action on the stomach suggest that melatonin may act as a modulator for 5-HT action on the gastrointestinal tract.

Animals↗
PubMed1989

Dual effects of zinc sulphate on ethanol-induced gastric injury in rats: possibly mediated by an action on mucosal blood flow.

The present study examines the protective effect of zinc sulphate against ethanol-induced gastric mucosal ulcers in rats. Absolute ethanol decreased the gastric mucosal blood flow and produced haemorrhagic lesions in the glandular mucosa. Zinc sulphate preincubation in an ex-vivo stomach chamber preparation prevented the formation of ethanol-induced lesions and attenuated the decrease of blood flow produced by ethanol. Subcutaneous injection of the same doses of the drug at 15 and 30 min before ethanol exposure, markedly reduced the blood flow and also aggravated ethanol-induced gastric injury; however, when injected at 23 and 24 h before ethanol administration, zinc sulphate protected against lesion formation but had no effect on the vascular changes induced by ethanol in the gastric glandular mucosa. These findings show that the antiulcer effect of zinc sulphate occurs only when the drug is given orally, or injected s.c. 23 and 24 h before ethanol challenge. Furthermore, this protective action is probably not entirely mediated by preservation of the gastric mucosal blood flow.

Animals↗
PubMed1989

The protective mechanisms of paracetamol against ethanol-induced gastric mucosal damage in rats.

The protective mechanisms of paracetamol against ethanol-induced gastric mucosal damage have been examined. The antiulcer action of subcutaneously (s.c.)-injected paracetamol, 250 mg kg-1, was attenuated by either subdiaphragmatic vagotomy or s.c. injection of N-ethylmaleimide, 10 mg kg-1. This attenuation was not seen in rats given paracetamol by the oral route (p.o.). Indomethacin pretreatment, 5 mg kg-1, did not influence the lesion-preventing action of paracetamol given s.c. or p.o. The findings suggest that the antiulcer effect of s.c.-administered paracetamol results from an action involving the vagal nerve and tissue sulfhydryls, but not prostaglandins. On the other hand, the protective mechanism of paracetamol p.o. is independent of the vagal system or tissue sulfhydryls and prostaglandins. It seems that paracetamol given p.o. exerts its antiulcer effect by acting directly on the mucosal cell to strengthen mucosal integrity.

Acetaminophen↗
PubMed1989

Effect of sucralfate on gastric mucosal blood flow in rats.

Sucralfate possesses site protective and cytoprotective actions and heals ulcers effectively, but its effect on gastric mucosal blood flow is unknown. Using an ex vivo gastric chamber preparation, we studied the effect of sucralfate on gastric mucosal blood flow in rats by laser doppler flowmetry. Under both fasting and fed states, measurements of gastric mucosal blood flow and damage were made in rats after topical application of absolute ethanol alone or after pretreatment with sucralfate. Gastric mucosal damage was assessed by measuring the total area of haemorrhagic mucosal lesions. Ethanol induced gastric mucosal lesions were significantly less with sucralfate pretreatment than without (p less than 0.008). Mucosal blood flow significantly fell after ethanol application (p less than 0.001). The fall was significantly less in fed than in fasted rats (p less than 0.05), and after pretreatment with sucralfate 100 mg or 200 mg than without in both fasted (p less than 0.0008 and 0.00001, respectively) and fed (p less than 0.002 and 0.001, respectively) rats. Graded doses of sucralfate (25-400 mg) resulted in an increase in gastric mucosal blood flow in a dose dependent manner (r = 0.731, p less than 0.001). In conclusion that sucralfate increases gastric mucosal blood flow in rats and lessens the fall in blood flow in rats treated with ethanol, and this action may contribute to its protection against the vascular damage of mucosa by ethanol.

Animals↗
PubMed1989

The possible role of metabolic acidosis in acetazolamide-induced gastric lesion formation in rats.

The effects of acetazolamide on blood acid/base balance and the relationship of the latter to gastric lesion formation were studied in rats. Acetazolamide (200 mg/kg, s.c.) produced haemorrhagic gastric lesions which were accompanied by lowered arterial blood pH and HCO3- levels. High dose (6.2%) of NaHCO3 infusion normalised the arterial blood pH and decreased lesion formation. It also markedly raised the blood HCO3- level. However, a lower dose (3.1%) of the drug only raised the HCO3- to a normal level and slightly reduced the severity of ulceration. These results suggest that metabolic acidosis is the main causative factor while depletion of blood HCO3- may play a minor role in acetazolamide-evoked lesion formation in rat stomachs.

Acetazolamide↗
PubMed1989

Gastric and cardiac organoprotection by lidocaine.

The concept of cytoprotection has been applied to many tissues afforded protection by drugs or endogenous chemicals against organelle, cyto- or histopathologic damage. We review here the "organoprotection" by lidocaine in rats and dogs as appraised by in vitro, ex vivo, and in vivo experiments with the stomach and heart, and as revealed at organelle to organ functional levels. Gastric mucosal lesions induced by 80% ethanol with 100 mM HCl on the ex vivo rat stomach were significantly reduced by lidocaine (2.2-4.4 mg/kg bolus followed by 66-132 micrograms/kg/min i. v. infusion). In anesthetized dogs with gastric corporeal lesions induced by increased gastric intraluminal pressure (50 mm Hg, 2.5 hrs), lidocaine (2.2 mg/kg bolus plus 66 micrograms/kg/min infusion) significantly reduced lesion severity. In the isolated rat heart, reperfusion after a 60 min period of ischemia induced localized cardiac mitochondrial swelling and disruption in ventricular apices which was greatly reduced if hearts were pretreated (15 min perfusion with lidocaine). In intact rats subjected to hemorrhagic shock, lidocaine pretreatment also facilitated shock resuscitation and reduced ultrastructural damage. In these diverse experiments, lidocaine organoprotection was likely mediated in part through reduction of ischemia induced organelle membrane damage and through reduction of reperfusion-induced superoxide and other oxygen-derived free radical related damage.

Animals↗
PubMed1988

Paracetamol confers resistance to ethanol-induced gastric mucosal damage in rats.

Paracetamol given orally or subcutaneously did not produce any observable gastric mucosal damage, nor did it change the acidity of the residual secretion in rat stomachs. However, it delayed the gastric emptying rate and increased the residual volume of gastric secretion. Pretreatment with paracetamol 250 mg kg-1 significantly prevented ethanol-induced gastric ulceration. Although it did not influence ethanol-stimulated acid secretion, it increased the mucosal mucus content in the ethanol-treated animals. The findings suggest that the protective mechanism of paracetamol against ethanol-induced damage is likely to be due to improved gastric mucosal integrity, through an increase in the adherent mucosal mucus which protects the underlying delicate cellular structures.

Acetaminophen↗