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Biomedical subjects

K Takagi

Publications and source records attributed to K Takagi.

At least 883 records · Page 49Linked to original sources
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

Relationship between the levels of intracellular cyclic nucleotides and mechanical responses induced by drugs.

The tracheal smooth muscle dissected free from connective tissues was used as a test preparation, since isoprenaline caused a decrease in cyclic GMP in the muscle while it caused an increase in cyclic GMP in the remaining tracheal tissue. Acetylcholine, histamine and papaverine increased both cyclic AMP and cyclic GMP levels in the tracheal muscle. Isoprenaline increased the cyclic AMP level but decreased the cyclic GMP level. However, when tracheal muscle was incubated with isoprenaline in the presence of acetylcholine, isoprenaline did not cause a decrease in cyclic GMP but rather a significant increase in cyclic AMP after only 1 min incubation. These results indicate that the relaxation of the tracheal muscle by isoprenaline is initiated by the increase in cyclic AMP but is not associated with the change in cyclic GMP.

Acetylcholine↗
PubMed1976

Effects of 5-hydroxytryptamine and morphine on the stomach motility in situ.

The effects of 5-hydroxytryptamine and morphine on the stomach motility were determined in in situ experiments. 5-Hydroxytryptamine and morphine inhibited stomach motility of unanaesthetized cats but did produce a slight contraction of the stomach of anaesthetized cats. In unanaesthetized rabbits, 5-hydroxytryptamine caused a contraction, followed by an inhibition of motility, and morphine depressed motility. The 5-hydroxytryptamine-induced contraction is a direct action on smooth muscle and the inhibition of spontaneous movement due to 5-hydroxytryptamine may be, in part, mediated through catecholamine-release and in part, result from paralysis of the receptors for 5-hydroxytryptamine in the cholinergic nerves in the stomach. In anaesthetized rabbits, 5-hydroxytryptamine produced contraction and morphine had no effect. In unanaesthetized guinea pigs, 5-hydroxytryptamine caused a contraction and morphine abolished spontaneous movement of the stomach. In anaestetized guinea-pigs, 5-hydroxytryptamine caused contraction and morphine produced no effect. The 5-hydroxytryptamine-induced contraction of the guinea pig stomach is indirect. From these results it is concluded that the differences in the modes of actions of 5-hydroxytryptamine and morphine on gastric motility are related to differences in species and experimental conditions such as anaesthesia.

Acetylcholine↗
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

Behavioral and physiological studies of seizures induced by systemic injection of metrazol in chickens.

The influence of systemically administered Metrazol on behavior, electroencephalogram and body temperature has been studied in young and adult chickens. Distinct convulsions were induced by 30--50 mg./kg. Metrazol administered intravenously in adults: they consisted of an initial excited state, a tonic convulsion accompanied with opisthotonos, and finally, convulsive movements. During recovery from these convulsions, three distinct behaviors were observed: violent peck-like movement, watchful state and finally panting behavior. All of the birds receiving higher intravenous doses (60--100 mg./kg.) exhibited vigorous convulsions immediately after injection and death occurred in 100% of the birds receiving these doses. An intraperitoneal injection of 75--100 mg./kg. Metrazol produced typical convulsions in young and adult chickens. At these doses, convulsions consisted of an initial excited state, a tonic convulsion accompanied with opisthotonos, and convulsive movements which involved clonic and tonic phases. The threshold for evoking typical convulsions with intraperitoneal injection ranges between 50 and 60 mg./kg. Metrazol in young chickens. The intravenous threshold doses for evoking high amplitude (1--2 mV.) in the EEG of adult chickens was 60 mg./kg. Metrazol. High intraperitoneal doses of Metrazol(75-100 mg./kg.) produced typical spikes with large amplitude which were synchronous in the two hemispheres in both young and adult chickens. There was a marked increase in body temperature within 10 minutes after injection in all cases of 50 mg./kg. intravenous dose: maximum increase (at 40 min.) was 1.5 degrees C. as compared with controls, however, it decreased rapidly with panting behavior. The highest does (100 mg./kg.) produced a maximum increase in body temperature of 3 degrees C. Discussion of epileptic seizure susceptibility to Metrazol in aves, in the light of phylogenesis, is discussed.

Animals↗
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↗