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Biomedical subjects

T Umeda

Publications and source records attributed to T Umeda.

At least 379 records · Page 21Linked to original sources
PubMed1976

Biliary elimination of diazepam in man.

The metabolism of 14C-5-diazepam has been studied in 5 patients with T tube biliary drainage. A single bolus of 40 to 50 muCi was given intravenously and blood, urine, and bile were analyzed from 5 to 14 days. The mean half-life of elimination from blood was 93.2 hr; the major metabolite noted in blood was N-desmethyl-diazepam. In urine the average recovery of radioactivity was 48.9% and consisted of 3 OH-diazepam, 4'OH-diazepam, and oxazepam. In bile the average recovery of radioactivity was 5.35% (corrected to a bile flow of 700 ml was 15.0%) and consisted of the same metabolites as in the urine. Essentially no diazepam or N-desmethyl-diazepam was found, and therefore an enterohepatic circulation cannot be held to account for the prolonged half-life of these substances in man.

Adult↗
PubMed1976

Effects of propranolo, itramin tosylate and dipyridamole on myocardial phosphate metabolism in anoxic perfused rat hearts.

Effects of propranolo, itramin tosylate and dipyridamole on coronary flow, cardiac activity and phosphate metabolism were investigated in anoxic perfused rat hearts. During anoxia, heart contractions showed a transient increase followed by gradual declines in amplitude and frequency, while ATP and creatine phosphate (CP) contents strikingly decreased accompanying a pronounced increase in inorganic phosphate (Pi). Propranolol added to the anoxic perfusate attenuated the decrease in CP and increase in Pi, whereas heart contractions wre more markedly depressed than by anoxia alone. Similar effects were also seen in electrically paced anoxic hearts. Itramin decreased ATP contents in non-paced anoxic hearts, but did not in paced ones. Dipyridamole did not produce any significant effect on phosphate metabolism in anoxic myocardium. It was considered that propranolol prevented the anoxia-induced reduction in high-energy phosphates by antagonizing catecholamines released by anoxia and that itramin decreased ATP level by inhibiting ATP generation.

Adrenergic beta-Antagonists↗
PubMed1976

Enhancement of sulphatide metabolism in the hypertrophied kidney of C3H/He mouse with reference to [Na+, K+]-dependent ATPase.

Sulphatide (cerebroside sulphate) metabolism of C3H/He mouse kidney was investigated in the course of compensatory renal hypertrophy in association with the change of [Na+,K+]-dependent ATPase, arylsulfatase A and beta-galactosidase activity. A remarkable increase in 35S incorporation into kidney sulphatide was observed 24 hours and especially 7 days after unilateral nephrectomy. In contrast, no significant alteration of 32P incorporation into major phospholipids such as phosphatidylcholine, phosphatidylethanolamine and sphingomyelin was demonstrated in the compensatory hypertrophied mouse kidney. [Na+, K+]-dependent ATPase increased to 126% of control in the remaining kidneys on 7 days after operation. Specific increase in 35S specific activity of kidney sulphatide suggests its possible link with the process of active ion transport through membrane-bound [Na+,K+]-dependent ATPase. Arylsulphatase A activity increased to 151% of control on days, while little change was observed in beta-galactosidase activity. These results suggest a sole concern of a turnover of sulphate moiety of sulphatide molecule in the elevated metabolism.

Adenosine Triphosphatases↗