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Biomedical subjects

M Takaki

Publications and source records attributed to M Takaki.

120 records · Page 7Linked to original sources
PubMed1979

Effects of vagotomy on feeding and defecation in guinea pigs.

The effect of subdiaphragmatic vagotomy on food intake and defecation was studied in guinea pigs. Weights of food and feces were measured for at least three weeks after vagotomy. The weight of daily food intake and feces evacuated increased about 15 and 30% after vagotomy compared with controls whereas it did not change in sham operated animals. The weight of scybalum decreased after vagotomy although the number increased markedly. It was considered that an increase in food intake after vagotomy may result from blocking of satiety signals mediated by the vagus; moreover, that the increase in feces may depend on the enhancement of scybalum formation in the proximal colon resulting from increasing food intake and transportation of the larger amount of the contents after vagotomy.

Animals↗
PubMed1975

[Effects of various agents and transmural electric stimulation on the motility of isolated bile duct of the dolphin (Stenella caeruleoalbus) (author's transl)].

The isolated bile duct preparations, which contain the duodenal circular muscle, and the proper bile duct muscle preparations in the dolphin (Stenella caeruleoalbus) were used and their longitudinal motilities were recorded by means of strain gauge transducer. 1. Raising the intraluminal pressure produced the augmentation of the motility of the bile duct preparation. 2. Acetylcholine and carbamylcholine caused the increase of the motility of the bile duct preparations. After atropinization the excitatory response was completely abolished. 3. Adrenaline caused the inhibitory response more predominantly than the excitatory one in the bile duct preparations, while in the proper bile duct muscle preparations it induced the excitatory response more predominantly than the inhibitory one. Phenylephrine produced mainly the excitatory effect in both preparations, while isoprenaline did chiefly the inhibitory one. These experimental results suggest that activation of alpha- and beta-adrenergic receptors in the bile duct muscle causes the excitatory and inhibitory responses, respectively. 4. Transmural electric stimulation induced both excitatory and inhibitory responses in the bile duct preparation. The former response was abolished after atropinization, while the latter one was not. It may be, therefore, suggested that the excitatory response was induced by stimulation of cholinergic neurons, while the inhibitory one was produced by that of the adrenergic fibers and non-adrenergic inhibitory neurons.

Acetylcholine↗
PubMedDate not supplied

Motor response secondary to the release of endogenous serotonin by tryptamine in guinea-pig ileal longitudinal muscle with adherent myenteric plexus.

The mechanism of the contractile action of tryptamine on the longitudinal smooth muscle with adherent myenteric plexus in the guinea-pig ileum was reexamined in view of new evidence that tryptamine releases the enteric neural serotonin (5-HT) and noradrenaline. The desensitization to 5-HT abolished the contractile response to tryptamine (5 and 10 microM). The contractile response to tryptamine (1-5 microM) was progressively decreased by repeated application. The progressive decrease by tryptamine was more pronounced than that by exogenous 5-HT. Tetrodotoxin and atropine significantly decreased the contraction upon the 2nd trial of tryptamine (5 microM) by about 40% and 45% of the control, respectively. However, guanethidine or cocaine did not change the contraction by tryptamine (5 microM). A 5-HT uptake inhibitor, zimelidine, which had been demonstrated to block the release of preloaded [3H]5-HT by tryptamine (Takaki et al., 1985), intensively reduced the contractile response to tryptamine to the same extent as atropine. These results are consistent with the previous finding that tryptamine releases the physiologically active 5-HT from myenteric neurons (Takaki et al., 1985). The 5-HT released by tryptamine, at least in part, acts on myenteric cholinergic neurons, resulting in the muscular contraction.

Animals↗