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Biomedical subjects

K Takagi

Publications and source records attributed to K Takagi.

At least 865 records · Page 48Linked 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

Mechanism of morphine block of electrical activity in ganglia of Auerbach's plexus.

A study was made of the effect of morphine on electrical activity within single ganglia of Auerbach's plexus of guinea pig longitudinal muscle-myenteric plexus as monitored by means of external electrodes. Morphine produces a concentration dependent block of single spike activity. This effect is competitively antagonized by naloxone. The ED50 for morphine effect is about 7 X 10(-7) M. Naloxone and dextrorphan have no effect on electrical activity. Acetylcholine in the concentration range of 10(-7)--10(-5) M augments electrical activity of ganglia. Morphine has little if any effect on the enhanced stimulation produced by acetylcholine thus indicating that the drug does not act directly upon the ganglion. Our results suggest that a specific opiate receptor is present on the preganglionic nerve terminals and that morphine and other opiates block ganglionic transmission by inhibiting the release of preganglionic acetylcholine.

Acetylcholine↗
PubMed1976

Histamine receptor-mediated calcium ion movement in a receptor-rich microsomal fraction.

The histamine receptor-rich microsomal fraction from the longitudinal muscle of cat small intestine, which consists of membrane vesicles, was loaded with 45Ca ions and the Ca ion efflux from it was examined. Histamine increased the efflux of 45Ca ions. The effect of histamine was blocked by diphenhydramine. Histamine had no effect on the histamine receptor-free microsomal fraction from dog small intestine muscle. This suggests that the ion movement may be mediated by histamine receptors.

Animals↗
PubMed1976

Effect of a cholinergic stimulant on interaction of isoprenaline with beta-adrenoceptors.

The maximum contraction induced in taenia from the guninea pig caecum by a cholinergic stimulant, butyltrimethylammonium (BuTMA) was relaxed by papaverine (10(-4) M) but not by l-isoprenaline (5 X 10(-7) M). The concentrations used relaxed the taenia completely in the absence of BuTMA. BuTMA (10(-4) M) decreased the increase of cyclic AMP caused by isoprenaline but not that due to papaverine. Futhermore, photoinactivation of the beta-adrenoceptors by l-isoprenaline was not observed on the taenia contracted by BuTMA (10(-4) M). These results suggest that l-isoprenaline does nto interact with the beta-adrenoceptors in the taenie contracted by the high concentration of BuTMA.

Animals↗
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↗