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Biomedical subjects

C H Cho

Publications and source records attributed to C H Cho.

At least 145 records · Page 8Linked to original sources
PubMed1993

Portal hypertension. Its effects on gastric function and ethanol-induced gastric mucosal damage in rats.

The time-course effects of portal hypertension on gastric secretory function, mucosal blood flow, vascular permeability, and ethanol-induced gastric mucosal damage were examined in anesthetized rats. Partial ligation of the portal vein effectively produced portal hypertension one to three days later but the raised pressure returned to normal on the sixth day after ligation. This time-course effect coincided with reduced pepsin secretion and mucosal blood flow and also with potentiated ethanol-induced mucosal damage during the first to third days. These effects started to tail off on the sixth day. However, gastric acid output was significantly reduced on the third day, and this was strongest on the sixth day after operation. Portal vein ligation also reduced basal vascular permeability, which was markedly potentiated after ethanol treatment. It is concluded that: (1) portal vein blood pressure changes are a time-dependent process following ligation; (2) changes in gastric mucosal blood flow (GMBF) and lesion formation are closely related to portal hypertension; (3) gastric mucosal injury is associated with vascular damage, as evidenced by increased in vascular permeability; and (4) pepsin but not acid secretion is closely related to the state of the GMBF.

Animals↗
PubMed1993

Effect of epidermal growth factor on gastric blood flow in rats: possible role in mucosal protection.

BACKGROUND: The mechanism by which epidermal growth factor (EGF) protects the gastric mucosa against injury is unclear. Whether EGF has any effect on gastric blood flow has not been reported. METHODS: Using an ex vivo gastric chamber preparation, the effect of EGF on gastric blood flow in rats was studied by laser Doppler flowmetry. Measurements of blood flow and mucosal damage were made in both intact and sialoadenectomized rats with graded doses of EGF at basal condition and after topical application of absolute ethanol. RESULTS: Sialoadenectomy alone increased ethanol-induced gastric mucosal lesions (P < 0.05) but had no significant effect on blood flow. EGF pretreatment resulted in both a reduction in ethanol-induced gastric mucosal injury as well as a significant increase in blood flow compared with controls (both P < 0.05). Graded doses of EGF (3.12-25 micrograms) resulted in an dose-dependent increase in gastric blood flow (r = 0.68; P < 0.001), which correlated inversely with the degree of mucosal damage (r = -0.72; P < 0.001). CONCLUSIONS: Mucosal protection by EGF is accompanied by an increase in gastric blood flow; this action may contribute to its mucosal protective effect.

Animals↗
PubMed1993

Adenosine and cholinergic-induced gastric contraction in rats.

Adenosine is known for its modulatory effects on gastric secretory function and mucosal blood flow in rats. However, its action on gastric motility has not been defined. The influence of adenosine on gastric contractions provoked by cholinergic drugs and direct vagal stimulation have, therefore, been examined. Bethanechol (25, 50 or 100 micrograms/kg i.v.) and electrical vagal stimulation dose and voltage dependently increased the number and the amplitude of gastric contractions. An adenosine-A1-receptor agonist, L-phenylisopropyladenosine (10 or 50 micrograms/kg s.c.), given 30 min beforehand, did not affect the changes in gastric parameters but decreased the basal mean blood pressure and lessened the reduction in blood pressure evoked by bethanechol. The adenosine-A2-receptor agonist N-ethylcarboxaminoadenosine (1 or 5 micrograms/kg s.c.), 30 min beforehand, however, significantly increased the number but not the force of gastric contractions; a lower dose of this drug increased the basal blood pressure and potentiated the depressive action of bethanechol on systemic blood pressure. Adenosine administration (7.5 mg/kg s.c.) significantly increased its plasma levels at 30 and 60 min after injection; pretreatment with it (2.5, 7.5 or 12.5 mg/kg s.c.), 30 min beforehand, did not affect the gastric and vascular actions of bethanechol. The highest dose of adenosine potentiated the contractile response of vagal stimulation. In the isolated fundus preparation, adenosine added to the organ bath (10(-6), 10(-4), 10(-2) M) also did not affect the contractions induced by acetylcholine.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenosine↗
PubMed1993

Nicotine and gastric ulcers in stress.

Chronic nicotine treatment worsens stomach mucosal damage by cold (4 degrees C) and restraint (stress): it dose- and time-dependently intensifies stress-evoked gastric glandular ulceration, mast cell degranulation and motility. Nicotine 50 micrograms/ml drinking water, given ad libitum to female Sprague-Dawley rats for 10 days, increases the sensitivity of the isolated stomach strip to acetylcholine-induced contractions; atropine abolishes this action. The isolated anococcygeus muscle from nicotine-treated male rats shows increased sensitivity to noradrenaline-induced contractions, but not to those by acetylcholine. Hexamethonium or atropine pretreatment antagonises stress-induced gastric effects in nicotine-drinking rats. Muscarinic M1- and M2-, but not M3-, receptor block (by pirenzepine, AF-DX 116BS and HHSiD, respectively) inhibits stress ulcer formation in female rats. Although tobacco smoking has been reported to increase free radical formation, mucosal xanthine oxidase which initiates free radical formation is uninfluenced by nicotine; antagonising this enzyme (by allopurinol) or hydroxyl free radical scavenging (by dimethylsulfoxide) does not lessen the effect of nicotine on stress-evoked ulceration. The findings suggest that chronic nicotine treatment produces partial ganglionic blockade of the vagal nerve which leads to muscarinic receptor supersensitivity. This phenomenon contributes significantly to the ulcer-worsening mechanism; muscarinic M1- and M2-receptors appear to be involved. The gastric ulcer-aggravating effect of nicotine in stressed rats appears not to be due to increased free radical formation.

Animals↗
PubMed1992

The influence of chronic nicotine treatment on stress-induced gastric ulceration and emptying rate in rats.

Ten-day treatment with nicotine (5, 25 or 50 micrograms/ml drinking water) dose-dependently intensified gastric ulceration induced by cold-restraint, and emptying rate. Stomach contractions produced by graded doses of bethanechol i.v. were elevated further by nicotine treatment. It is suggested that chronic nicotine administration produces hypersensitivity of the gastric muscarinic receptors; stomach hypermotility contributes to the ulcer-worsening action of the alkaloid.

Animals↗
PubMed1992

The inhibitory action of ethanol on the gastric mucosa and its interaction with the vagus in rats.

The influence of systemic ethanol and/or the vagus on ionic secretion and on glandular mucosal blood flow (GMBF) was studied in an ex-vivo gastric chamber preparation in rats. Sub-diaphragmatic vagotomy decreased H+ secretion and Na+ outflux from the gastric mucosa. Subcutaneous injection of 50% ethanol significantly potentiated these responses, but not the concentrations of 25% and 100%. The three doses of ethanol did not affect the secretion of both H+ and Na+ in vagus-intact animals. Ethanol, however dose-dependently reduced the GMBF in both vagus-intact and sub-diaphragmatic vagotomised rats, and the effect was greater in the latter-operated animals. It is concluded that vagus nerves greatly influence the secretion of both H+ and Na+ the gastric mucosa but the effect is unrelated to GMBF. Systemic ethanol reduced the secretion of these ions only in vagotomised animals, indicating the vagus could play a role in modulating the action of ethanol in the stomach.

Animals↗
PubMed1992

The pharmacological differences and similarities between stress- and ethanol-induced gastric mucosal damage.

Stress- and ethanol-induced gastric mucosal damage are the two commonly used ulcer models in animals. They share some of the similarities but also have differences in the etiology of gastric ulceration. This article reviews the influences of various protective drugs on these two types of gastric damage in rats. Verapamil (a calcium antagonist) or N-ethylmaleimide (a sulfhydryl depletor) prevents cold restraint-, but potentiates ethanol-provoked gastric lesion formation. N-Acetylcysteine (a mucolytic agent) and acetaminophen (an antipyretic analgesic) have the opposite actions. Prostaglandins provide a much better antiulcer effect on ethanol-induced lesions. Cimetidine (a histamine H2-receptor antagonist) prevents only stress-induced mucosal damage. These differences in drug actions indicate that stress and ethanol may have dissimilar ulcerogenic mechanisms in rats. On the other hand, carbenoxolone (a mucus inducer), histamine H1-receptor antagonists, leukotriene inhibitors (FPL 55712 and nordihydroguaiaretic acid) and mast cell stabilizers (like zinc compounds, sodium cromoglycate, FPL 52694 and ketotifen), all protect against gastric mucosal damage by stress or ethanol in rats. However, the role of gastric sulfhydryls in both types of gastric lesions is still controversial. These findings imply that the two types of lesion formation share some of the ulcerogenic mechanisms. This communication attempts to analyze the various findings and to relate them to the etiology of stress and ethanol-induced gastric lesions. It also summarizes the uses, and the antiulcer mechanisms, of the drugs that have been studied utilizing these two animal ulcer models, and suggests their possible implications in man.

Acetaminophen↗
PubMed1992

Effects of nicotine on activity and stress-induced gastric ulcers in rats.

Nicotine is known to influence locomotor activity. The alkaloid also intensifies gastric ulcer formation in stressed rats. The effects of nicotine on locomotor activity in relation to gastric lesions induced by restraint at 4 degrees C for 2 h (stress) were, therefore, studied. Ten-day treatment with nicotine 25 or 50 micrograms/ml drinking water potentiated stress-evoked ulceration and mast cell degranulation. These same doses of nicotine increased vertical motor activity; only the higher dose of the alkaloid enhanced horizontal movements. Phenobarbitone (12.5, 25, or 50 mg/kg, SC) dose dependently reduced vertical activity, as well as stress-induced gastric ulceration and mucosal mast cell degranulation. The drug also lessened the potentiating effects of nicotine on motor activity and stress-evoked gastric lesion formation. It is concluded that the ability of chronic nicotine treatment to intensify stress-induced gastric ulceration most likely owes part of its action to a mechanism evoking increased activity, which possibly reflects an influence on the CNS, as well as to enhancement of mast cell degranulation in the stomach glandular mucosa.

Animals↗
PubMed1992

A correlative study on serum cholylglycine levels in hepatobiliary disease.

The serum cholylglycine (CG), alanine aminotransferase (ALT) and total bilirubin levels were studied in 210 patients with hepatobiliary disease and in 70 healthy subjects. Serum CG concentrations in all the hepatobiliary diseases were found to be significantly higher than those of their controls. Patients with abnormal increases in ALT and bilirubin levels also showed raised CG concentrations; however, some patients with normal ALT and bilirubin levels, still had markedly elevated CG values. Patients with hepatic cirrhosis had high serum CG levels, followed, in descending order, by chronic active hepatitis and chronic persistent hepatitis. In the cholecystitis and cholelithiasis cases, their CG levels were significantly higher than those of the controls but lower than the values in hepatic disease patients; however, more cholecystitis cases had abnormally high serum bilirubin levels than CG. The results also show that serum CG concentrations vary in the different hepatobiliary diseases, and that serial CG measurements are more sensitive than measuring ALT and bilirubin levels in the diagnosis of hepatic diseases. Serum CG can be used as an index for evaluating the activity of chronic hepatitis; it can also be employed as a diagnostic tool in cholecystitis and cholelithiasis.

Adolescent↗
PubMed1992

The cytoprotective effect of zinc L-carnosine on ethanol-induced gastric gland damage in rabbits.

The effects of zinc L-carnosine on the damaging actions of ethanol were examined in rabbit isolated gastric glands. Ethanol (8%, v/v) incubation produced a 50% viability of the gland populations and released a significant amount (38%) of the total lactate dehydrogenase (an index of membrane injury) of the glands. Zinc L-carnosine pre-incubation for 15 min markedly prevented these actions of ethanol; however, L-carnosine by itself did not have these effects. The findings indicate that zinc ion but not carnosine in the zinc L-carnosine molecule possesses cytoprotective action against ethanol-induced gastric gland damage in rabbits.

Animals↗
PubMed1992

Polyethylene glycol: its adverse gastric effects in rats.

The effects of polyethylene glycol (PEG) on gastric function and on lesion formation, evoked by topical applications of absolute ethanol to an ex-vivo stomach chamber preparation have been examined. Parenteral injection (i.p. or s.c.) of PEG with different molecular weights (PEG 300, 400 or 4000), dose-dependently reduced the gastric mucosal blood flow and volume of gastric secretion; these effects were greater in rats given PEG by the i.p. route, which also lowered acid output. Topical application of 1.5 mL absolute ethanol produced severe gastric mucosal injury, which was exacerbated by PEG; this lesion-aggravating effect was higher in the i.p.-injected groups. These findings indicate that when PEG is given by injection, it can adversely affect gastric function and increase the damaging action of alcohol. It is suggested that the use of PEG as a vehicle for injection should be re-assessed.

Animals↗
PubMed1992

Chronic nicotine intake increases the responses to muscarinic receptor stimulation.

Chronic nicotine administration depresses the autonomic ganglia, but its effects on the muscarinic receptors at the neuroeffector sites remain unclear. The present study, using rats, examines the influence of chronic treatment with nicotine (25 micrograms/ml drinking water) for 10 or 15 days on muscarinic receptor responses, as reflected by bethanechol-evoked gastric secretion or by acetylcholine-induced decreases in mean blood pressure. Bethanechol, 0.4, 0.8, 1.6 or 3.2 mg/kg injected subcutaneously, dose-dependently increased the basal gastric secretory volume and acid output in pylorus-ligated control animals which normally drank tap water. Rats given nicotine in their drinking water for 10 or 15 days showed a further marked increase in both the volume of gastric secretion and acid output in response to bethanechol injections. Although bethanechol dose-dependently increased acid secretion, the ulcer index was very small and there was no significant difference between the control and nicotine-treated groups. The basal mean blood pressure remained normal after the 10-day nicotine treatment. Acetylcholine, 0.1, 0.3, 1 or 3 micrograms/kg given intravenously, decreased the mean blood pressure; this acetylcholine-evoked blood pressure fall was intensified by nicotine pretreatment. The findings suggest that the responses to muscarinic receptor stimulation are increased by chronic nicotine treatment for 10 or 15 days. These exaggerated effects are possibly the consequence of persistent autonomic ganglion blockade by chronic nicotine treatment.

Acetylcholine↗
PubMed1992

Ethacrynic acid and sulphasalazine inhibit the generation of leukotriene C4 in rat stomachs: a possible gastric anti-ulcer mechanism in cold-restraint-stressed rats.

The role of gastric glandular mucosal leukotriene C4 in gastric ulceration, produced by restraint at 4 degrees C (stress) for 2 h in rats, was studied in relation to the ulcer-preventing effects of ethacrynic acid, sulphasalazine and its constituents (sulphapyridine and 5-aminosalicylic acid), AA-861 and ONO-1078. Stress itself significantly raised mucosal leukotriene C4 levels; pretreatment with ethacrynic acid, sulphasalazine, sulphapyridine or AA-861 antagonised these changes and reduced the severity of gastric ulceration. Mucosal mast cell degranulation was prevented by ethacrynic acid, sulphasalazine, 5-aminosalicylic acid, AA-861 or ONO-1078; the mucus-depleting effect of stress was also reversed by all these drugs, except for 5-aminosalicylic acid. The anti-ulcer effect of ethacrynic acid and sulphasalazine appears to be related to their influence on glandular mucosal leukotriene C4 levels.

Animals↗
PubMed1992

Time course study on the action of 5-hydroxytryptamine on gastric secretion and mucosal blood flow and on ethanol-induced gastric mucosal damage in rats.

The effects of 5-hydroxytryptamine (5-HT; given i.p. in doses of 1 or 10 mg/kg) on gastric secretion and mucosal blood flow (GMBF) and on ethanol-induced gastric mucosal damage were studied in rats over a period of 30-450 min. The blood pressure was also examined, in relation to the changes in GMBF. 5-HT, 10 mg/kg, given 30 min before ethanol administration markedly worsened lesion formation and this potentiating action was present for a further 90 min; a significant protective effect was seen only at 450 min after 5-HT injection. The lower dose of 5-HT, 1 mg/kg, did not affect the severity of gastric damage. 5-HT (10 mg/kg) also decreased GMBF at 30 min after injection and this lasted up to the end of 120 min, but the depressive action of ethanol on GMBF was reversed at 450 min. The basal gastric secretory volume was depressed from 30 to 120 min but acid output fell from 75 to 120 min after the higher dose of 5-HT; this reduction of acid secretion was followed by an increase from 360 to 450 min. 5-HT decreased the mean blood pressure in a dose- and time-dependent manner. The heart rate was unaffected by either dose level of 5-HT. The present study not only demonstrates the ulcerogenic action of 5-HT but also the protective nature of the amine. The reduction in secretory volume and lesion formation, but not acid secretion, seems to be related to GMBF depression, whereas the protective action depends on the maintenance of GMBF.

Animals↗
PubMed1992

Natural killer activity and antibody-dependent cellular cytotoxicity in patients with primary lung cancer.

The NK activity and ADCC of peripheral blood mononuclear cell were examined to evaluate the contribution of ADCC and NK activity to host immune response against lung cancer. The NK activity and ADCC were examined in 58 patients with primary lung cancer and 40 healthy volunteers as normal controls. The NK activity of patients with lung cancer was significantly subnormal, but ADCC was at a normal level. The NK activity was decreased in non-small cell lung cancer (NSCLC), but not in small cell lung cancer (SCLC) compared to normal controls. According to stage, the NK activity in stage II, III-M0 and III-M1 NSCLC showed low levels compared to that of stage I NSCLC, but there was no difference of NK activity in patients with SCLC. The NK activity was not affected by performance status. There was no significant difference of ADCC in patients with lung cancer according to cell type, stage and performance compared with that of normal controls. The NK activity and ADCC were not changed after chemotherapy and operation respectively.

Antibody-Dependent Cell Cytotoxicity↗
PubMed1992

Surgical intervention in patients with aplastic anemia.

Eighteen surgical procedures have been performed on 14 cases of aplastic anemia (AA). Of the 10 major surgical procedures, 7 were emergency and 3 elective. The median duration from the diagnosis of AA to major surgery was 0.5 months (3 days-47.3 months), and the median survival after surgery was 12.3 months (4 days-38 months). The hematological status of AA at the time of major surgery were 3 in partial response (PR), 2 with no response (NR) and 5 at diagnosis, respectively; and those after major surgery were 2 with complete response (CR), 2 in PR, 1 with minimal response, and 2 in NR. Three postoperative complications were sepsis, pneumonia and atelectasis encountered in 2 cases. A total of 3 deaths were caused by infection and cancers. Considering the fact that surgery may not only control complications, but offer the opportunity to give effective therapy for AA and therefore improves chances for survival, it is strongly suggested that active surgical intervention should be performed if the patient's status is not terminal.

Adolescent↗
PubMed1992

Congenital absence of gallbladder.

Nine surgically proven congenital absence of gallbladder (CAGB) cases were reviewed. All of them had one or more kinds of biliary symptom. Tests such as abdominal ultrasonography, intravenous or oral cholecystography and even endoscopic retrograde cholangiography not only failed to predict CAGB but misleadingly indicated other similar conditions. Only the abdominal computed tomography (CT), performed on one patient, enabled the accurate diagnosis of CAGB. All the patients underwent abdominal exploration, and CAGB was confirmed by the meticulous dissection of the entire extrahepatic biliary tree and the operative cholangiography. Five patients had concomitant biliary pathologies responsible for their symptoms, but four patients had isolated CAGB. CAGB is a rarely encountered condition for a clinician, but extensive diagnostic work-ups including abdominal CT should be performed in all situations where CAGB is suspected. Thus unnecessary exploration can be avoided in the isolated CAGB case.

Bile Duct Diseases↗