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Biomedical subjects

S Okabe

Publications and source records attributed to S Okabe.

At least 541 records · Page 30Linked to original sources
PubMed1976

[Findings in the gastric mucosa and gastric secretion in rats treated with methyl O-(4-hydroxy-3-methoxycinnamoyl)reserpate (CD-3400) and reserpine derivatives].

CD-3400 developed by Nippon Chemiphar Co. Ltd., is a new antihypertensive agent belonging to the class of rauwolfa alkaloids. Influence of the agent on gastric mucosa, healing process of acetic acid-induced gastric ulcer and gastric juice in rats was investigated and compared with effects of reserpine and rescinnamine. CD-3400-induced gastric lesions were fewer in number than those produced with reserpine and rescinnamine in fasted rats. After a three day treatment of CD-3400 to fed rats, however, there were few gastric lesions, while reserpine- and rescinnamine-induced gastric lesions were aggravated to a greater extent that when a single administration was given to fasted rats. Influence of CD-3400, reserpine and rescinnamine on the healing process of acetic acid-induced ulcer was insignificant, but treatment with high doses of reserpine and rescinnamine resulted in death. Pretreatment with CD-3400 and reserpine produced a decrease in gastric acid and K+, and an increase in Na+. Repeated administration of reserpine for 5 days resulted in a decrease of both gastric volume and acid, while such was not seen with CD-3400. Treatment with anticholinergic agents such as atropine sulfate and atropine methylbromide inhibited CD-3400- and reserpine-induced gastric lesions. From these results, it would appear that cholinergic factors play a role in the pathogenesis of CD-3400-induced gastric lesions, as in the case with reserpine, and that the responses of these lesions to reserpine and CD-3400 correlate with changes of ionic fluxes in gastric juice.

Acetates↗
PubMed1976

Effects of various amino acids on gastric lesions induced by acetylsalicylic acid (ASA) and gastric secretion in pylorus-ligated rats.

The simultaneous oral administration of various amino acids such as L-lysine, L-arginine, L-histidine, L-serine and others at 750, 250 or 83.3 mg/kg in pylorus-ligated rats produced a marked prevention of the gastric mucosal damages caused by oral acetylsalicylic acid (ASA) at 100 mg/kg. In regard with L-lysine and L-arginine, it was assumed that these amino acids might inhibit the ASA-induced gastric lesions through neutralization of acid because of the high alkalinity of these amino acids. In addition, the lesser effect of the hydrochoride salts of these amino acids as compared with the free form on ASA-induced gastric lesions was observed. The other effective amino acids markedly prevented the back diffusion of acid in response to ASA, suggesting as one of the possible mechanisms of lesion formation. However, L-cysteine, which exerted insignificant effect on ASA-induced gastric lesions, also prevented the back diffusion of acid even though the Na+ concentration had not returned to the control level.

Amino Acids↗
PubMed1975

Inhibitory effect of L-glutamine on gastric irritation and back diffusion of gastric acid in response to aspirin in the rat.

L-Glutamine given orally at 750 mg/kg significantly reduced the formation of gastric mucosal lesions induced by aspirin at 100 mg/kg at 1, 3, and 7 hours in pylorus-ligated rats. L-Glutamine markedly inhibited the loss of H+ and a corresponding increment of Na+ through the aspirin-damaged mucosal barrier, which suggests inhibition of acid back diffusion as the mechanism of action. In vagotomized rats, the diffusion of H+ from the instilled acid solution into the gastric mucosa and outflux of Na+ from the mucosa into the lumen was so strong that aspirin could not show any acceleration of a back diffusion of H+ in contrast to the aspirin-free group. However, L-Glutamine given with or without aspirin inhibited the group. However, L-Glutamine given with or without aspirin inhibited the back diffusion of H+ instilled into the vagotomized rat stomach.

Animals↗
PubMed1975

Influence of the proximal small intestine on the gastric hypersecretion in pylorus-ligated rats.

The mechanism of the gastric secretory inhibition caused by the simultaneous ligation of the upper and lower duodenum or the jejunum in pylorus-ligated rats was studied. The data obtained from the experiments on surgical manipulation of the small intestine indicated that the absorption of certain substances appeared to be important in maintaining gastric secretion of pylorus-ligated rats. The participation of biliary secretion was negligible, while the ligation procedure per se, which results in the accumulation of duodenal contents, might be partly involved in the mechanism of acid secretion. Pharmacological techniques suggested that the inhibition appeared to be independent of cholinergic nervous reflex and hormonal influence, which is assumed to be released by intestinal acidification.

Animals↗
PubMed1975

Effects of L-glutamine on acetylsalicylic acid-induced gastric lesions in normal and cirrhotic rats.

Cirrhosis of the liver in rats was induced by the administration of carbon tetrachloride (0.1 ml/100 g of body weight, s.c.) biweekly for 13 weeks. In the pylorus ligation preparation, acetylsalicylic acid (ASA) 100 mg/kg p.o. induced much more serious gastric damage in CC14-induced cirrhotic rats as compared with rats with a normal liver. L-glutamine 750 mg/kg p.o. prevented the ASA-induced gastric lesions in both normal and cirrhotic rats, even though the degree of the inhibition was weaker in cirrhotic rats. Gastric analysis indicated that L-glutamine 750 mg/kg p.o. markedly inhibited the gastric ionic changes (acid back diffusion) in response to ASA in both cirrhotic and normal rats.

Animals↗
PubMed1974

Influence of L-glutamine on aspirin-induced gastric lesions and absorptions as well as antipyretic, analgesic and anti-inflammatory effects of aspirin in rats and mice.

L-glutamine markedly suppressed the development of the gastric lesions induced by aspirin in pylorus-ligated rats. In non-ligated normal rats, aspirin was absorbed rapidly after administration and was maintained in the blood in high salicylate concentration thereafter. When aspirin was administered in combination with L-glutamine, the absorption of aspirin was at nearly the same level as when aspirin had been given alone. In pylorus-ligated rats, administration of aspirin was followed by slow increment in blood salicylate concentration. Blood salicylate level in these rats was higher when aspirin was administered in combination with L-glutamine than when it had been given alone. Combined administration of aspirin and L-glutamine produced little influence on the antipyretic, analgesic and anti-inflammatory effects of aspirin in non-ligated normal rats.

Administration, Oral↗