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Biomedical subjects

K Takeuchi

Publications and source records attributed to K Takeuchi.

At least 1,405 records · Page 78Linked to original sources
PubMed1976

Effects of carbenoxolone Na on acute and chronic gastric ulcer models in experimental animals.

Effects of carbenoxolone Na on acute or chronic types of gastric lesions or ulcer models produced in rats, guinea pigs, or dogs were studied. Carbenoxolone Na, given either orally or intraperitoneally, produced a significant inhibition of stress-induced gastric lesions in intact or in pylorus-ligated rats. Acetylsalicylic acid (ASA)-induced or serotonin-induced gastric lesions in rats were also inhibited significantly by pretreatment with the drug. However, carbenoxolone Na did not affect the development of Shay ulceration in rats even though the peptic activity in gastric juices was markedly reduced by the drug. Histamine-induced gastric lesions in guinea pigs were not prevented by pretreatment with carbenoxolone Na. Although carbenoxolone Na, given for 10-20 days, did not promote the healing of stress-induced gastric lesions and acetic acid gastric jlcers in rats, it significantly accelerated the healing of chronic gastric ulcer produced in dogs by 3 weeks' treatment. Carbenoxolone Na prevented the acid back-diffusion caused by ASA without any influence on Na+ efflux in pylorus-ligated rats.

Acute Disease↗
PubMed1976

Influence of pregnancy on the development of various gastric lesions in rats.

The influence of pregnancy, and to some extent lactation, on various gastric lesions in rats were studied. Shay ulceration and gastric lesions induced by cold-restraint stress and ulcerogenic agents, such as acetylsalicylic acid (ASA), reserpine, or epinephrine, in rats were significantly aggravated by pregnancy (day 20 of pregnancy). Gastric hypersecretion, which was observed during pregnancy in pylorus ligation preparation, appears to contribute to the mechanism of aggravation of gastric lesions. ASA induced a marked back-diffusion of acid in pregnant rats which might resulted in the aggravation of ASA-induced gastric lesions. In contrast, histamine-induced gastric lesions were markedly inhibited according according to the progress of pregnancy but after 10 days' lactation returned to the level seen in nonpregnant rats. The histaminase inhibitor aminoguanidine strongly aggravated the histamine-induced gastric lesions in pregnant rats as compared with the non-pregnant ones.

Animals↗
PubMed1976

A new model of stress ulcer in the rat with pylorus ligation and its pathogenesis.

Water-immersion stress for 7, 14, or 20 hr consistently induced linear or punctate stress ulcers (mucosal erosions) in the corpus of the stomach in intact rats. When the pylorus of the stomach had been ligated prior to stressing, the stress ulcers changed their morphological feature (mainly punctate and in one place elongated) and location (both in corpus and antrum). Histologically, the stress ulcer developed in the proximal antrum of pylorus ligated rats and penetrated into the muscularis mucosa. Sodium bicarbonate, chlorpromazine, hexamethonium, atropine, metiamide, and bilateral vagotomy markedly inhibited the stress ulcers which developed in the pylorus-ligated rats. Phentolamine and propranolol hardly affected the development of stress ulcers. Amylopectine evoked a new type of stress ulcer in the corpus when it was given to the pylorus-ligated rats.

Amylopectin↗
PubMed1976

Intrathecal pharmacotherapy in coma.

A study was made of intrathecal infusion as a route for administration of drugs for the CNS. We recognize the presence of blood brain and CSF brain barriers. CDP-choline was used as the brain activator, and the effect of the intrathecally infused drug was investigated clinically. Fifteen patients with disturbances of consciousness due to primary cerebral lesions received a total of 39 intrathecal infusions of CDP-choline, and were examined neurologically and electroencephalographically before and after treatment.

Adult↗
PubMed1976

Effects of acetylsalicylic acid (ASA), ASA plus L-glutamine and L-glutamine on healing of chronic gastric ulcer in the rat.

A chronic gastric ulcer model was produced in rats by the subserosal injection of 20% acetic acid solution (0.015 ml) in order to examine whether (1) acetylsalicylic acid (ASA) irritates the chronic gastric ulcer in active or healed or diminished stage, (2) L-glutamine, given together with ASA, inhibits the adverse effect of ASA. Oral ASA 200 mg/kg/day, given in two divided doses for 10 consecutive days, apparently delayed the healing of the gastric ulcer and irritated the healed ulcer to reulcerate. L-Glutamine, 1,500 mg/kg/day, which was given together with ASA in two divided doses, markedly protected the gastric ulcer both in active and healed stages from the deleterious activity of ASA.

Animals↗
PubMed1976

Effects of L-glutamine on various gastric lesions in rats and guinea pigs.

Effects of L-glutamine on gastric lesion models in rats and guinea pigs were studied. Shay ulceration in rats was not inhibited by oral L-glutamine. Although stress-induced gastric lesions in intact rats were not inhibited by L-glutamine, a strong antagonism of gastric lesions was induced in pylorus-ligated rats under the same stress by the amino acid. Histamine-induced gastric lesions in intact rats and guinea pigs were also markedly inhibited by L-glutamine. L-Glutamine inhibited the gastric lesions in rats induced by compound 48/80 but not significantly. Reserpine- or serotonin-induced gastric lesions in rats were not affected by L-glutamine. The mechanism of L-glutamine protection was discussed.

Animals↗
PubMed1976

Effects of L-glutamine of acetylsalicylic acid or taurocholic acid-induced gastric lesions and secretory changes in pylorus-ligated rats under normal or stress conditions.

An oral dosing of either acetylsalicylic acid (ASA) or taurocholic acid (TCA) to pylorus-ligated rats subjected to water-immersion stress produced severe damage to the gastric musoca in contrast to the irritation observed in non-stressed ones. The irritative activity of ASA or TCA on gastric mucosa under stress was dose-dependent. Stress itself (23 degrees C, 7 hr) did not induce any appreciable changes in gastric mucosa under stress wasic mucosa of rats. L-glutamine, given together with SAS or TCA, significantly prevented the potentiated development of SAS- or TCA-induced gastric lesions in stressed rats. L-glutamine also prevented in varying degrees the reduction of acid and increment of Na+ ion in gastric juice accumulated in stressed rats in response to ASA or TCA.

Animals↗
PubMed1976

Effects of L-glutamine on acetylsalycylic acid induced gastric lesions and acid back diffusion in dogs.

Effects of L-glutamine on acetylsalicylic acid (ASA)-induced gastric mucosal lesions were studied in mongrel dogs. It was confirmed that when oral ASA at 1.0 or 2.0 g per dog is given in two divided doses, there is severe and consistent dose-dependent mucosal damage in the glandular portion of the stomach in fasted dogs. However, when L-glutamine 2.0 or 4.0 g per dog in two divided doses is given concomitantly with ASA 2.0 g per dog orally, the gastric irritation is significantly inhibited. Instillation of 20 mM of ASA in 100 mM HCl solution into the Heidenhain pouch of Beagle dogs produced a significant loss of H+ from the pouch and a gain of Na+ in the lumen compared with ASA-free controls. When L-glutamine (100 mM) was given concomitantly with ASA (20 mM) into the pouch, changes of electrolyte fluxes in response to ASA alone were significantly suppressed. However, 50 mM of L-glutamine had no appreciable effect on acid back diffusion caused by ASA 20 mM. The amino acid itself had little effect on the ionic movement in the pouch. Gross bleeding from the pouch treated with ASA was never observed with the concomitant dosing of ASA and L-glutamine 50 or 100 mM.

Animals↗
PubMed1976

[Efficiency of microbe filtration of air filter for rearing germfree animals (author's transl)].

Filtration efficiency of 3 types of air filter frame and cylinder (Fig. 1) was examined by culture of the air obtained from the operating isolators at intervals of 3 to 21 days. The air of isolator was bubled in 30 ml of nutrient broth for 30 or 120 minutes (4approximately15 l/min.) and each of 1 ml of the broth was inoculated into thioglycollate medium (TGC), cooked meat medium (CMM), heart infustion broth (HIB) and glucose peptone water (GPW). The media were incubated for 7 to 14 days at 30 or 25 degrees C. As seen in Table 1, microbes could be effectively removed through all types of filter for over 10 months, though there were a very few positive cases suggesting technically acidental contamination at sampling.

Air Microbiology↗
PubMed1976

[Clinicopathological studies of the vegetative state--distinction between the vegetative state and brain death].

10 cases showing vegetative state and 2 cases of brain death due to severe brain damage were observed and the differences of clinicopathological findings between both states were discussed. The cases of vegetative state can be divided into three groups, first is widespread lesion in the cerebral cortex, second is in the cerebral white matter and third is in the brain stem. While, the diffuse whole brain damage including the vegetative center of the central nervous system causes brain death. We should like to emphasize that the most important structure to maintain the human life is the vital center in the brain stem, and that a human being, in whom only those function can be preserved, is possible to be alive as vegetative state. Prognostic value of the EEG indicating quality of survival noted in early stage after severe brain damage has not so important as the flat EEG revealed in brain death.

Adult↗
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↗