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T Tateyama

Publications and source records attributed to T Tateyama.

33 records · Page 2Linked to original sources
PubMed1994

[Myocardial metabolism, oxygen demand and oxygen supply during prostaglandin E1 induced hypotension].

The effects of hypotensive anesthesia induced by PGE1 on myocardial metabolism, oxygen demand and oxygen supply were studied. Nine mongrel dogs were anesthetized with pentobarbital and isoflurane. Mean blood pressure (MBP), cardiac output (CO), blood gases (BG), coronary blood flow (CBF), and myocardial tissue oxygen tension (MPO) were measured. Arterial and coronary venous lactate and pyruvate concentrations were also measured. We calculated myocardial oxygen consumption, L/P ratio, excess lactate, oxygen extraction ratio and lactate extraction ratio to estimate the adequacy of myocardial aerobic metabolism. CO and CBF decreased in accordance with MBP depression. Myocardial oxygen consumption decreased significantly with PGE1 administration. Lactate and pyruvate concentrations, L/P ratio, excess lactate and myocardial tissue oxygen tension were unchanged. These results suggest that PGE1 exerts no significant effect on myocardial metabolism during hypotensive anesthesia.

Alprostadil↗
PubMed1994

[The effects of adenosine-induced hypotension on myocardial metabolism].

The effects of hypotension induced by adenosine on myocardial metabolism were studied in ten mongrel dogs anesthetized with 0.5% isoflurane. Adenosine was infused intravenously to reduce mean arterial blood pressure by approximately 30% during a period of 20 min. Although heart rate was unchanged, cardiac output increased and coronary blood flow increased 3-fold of the preinfusion value. Oxygen tension of the myocardium, and oxygen extraction as well as lactate extraction of the myocardium decreased. Myocardial oxygen uptake and myocardial lactate uptake were unchanged, but lactate production was observed in three of ten dogs. In addition, coronary venous lactate/pyruvate ratio and excess lactate increased, and excess lactate became positive in five of ten dogs. The results suggest that adenosine-induced hypotension may inhibit the myocardial aerobic metabolism.

Adenosine↗
PubMed1994

[Effect of 10% carbon dioxide on regional myocardial tissue oxygen tension and myocardial metabolism].

We investigated the effects of arterial carbon dioxide tension on myocardial blood flow, tissue oxygen tension and metabolism in the anesthetized dogs. Eighteen adult mongrel dogs weighing 13.4 +/- 3.6 kg were anesthetized with 0.5% isoflurane, intubated and ventilated mechanically with 50% oxygen to maintain normocapnia. Endtidal CO2 fraction (FECO2) was monitored continuously by capnograph. Regional myocardial tissue PO2 was measured using a monopolar polarographic needle electrode inserted to the myocardium. Electromagnetic blood flow probes were applied on the left anterior descending artery and circumflex artery. For cardiac venous blood sampling, a 23G intravenous catheter was inserted into the cardiac veins (great coronary veins) carefully. After normocapnic ventilation, hypocapnia was induced by increasing the respiratory rate, and hypercapnia was induced by adding 10% carbon dioxide to the inspired gas. The coronary blood flow and myocardial tissue oxygen tension increased during hypercapnia and the myocardial lactate extraction decreased, while excess lactate and cardiac venous L/P ratio increased during hypercapnia. These results indicate that hypercapnia increase coronary flow and myocardial tissue oxygen tension but myocardial aerobic metabolism is impaired during hypercapnia.

Anesthesia, Inhalation↗
PubMed1992

[Effect of hypotensive anesthesia on tissue oxygen tension of the heart, kidney and liver].

The effects of hypotensive anesthesia by prostaglandin E1 (PGE1: 8 dogs) or trimetaphan (TMP: 8 dogs) on tissue oxygenation were studied in 16 mongrel dogs anesthetized with pentobarbital. Mean blood pressure (MBP), heart rate (HR), cardiac output (CO), blood gases (BG), the blood flow and tissue oxygen tension of the heart, the kidney and the liver were measured. The blood flow and oxygen tension were measured by electromagnetic flowmeters and by polarographic oxygen electrodes respectively. PGE1 or TMP was injected intravenously to decrease MBP by 30%. MBP, CO, HR and BG of PGE1 were not significantly different with those of TMP. Coronary blood flow decreased for 12% with PGE1 and for 33% with TMP. Though blood flows of the renal and the hepatic arteries were well maintained with PGE1, they decreased for 36% and 34% respectively with TMP. Oxygen tensions of the myocardium (both outer and inner layers) and the liver were well maintained with PGE1. But with TMP, oxygen tension decreased for 23% in outer layer, for 16% in inner layer and for 31% in the liver. Oxygen tension of the kidney remained unchanged with PGE1 and TMP. The results suggest that PGE1 is more useful for the maintenance of the tissue oxygenation than TMP during hypotensive anesthesia.

Anesthesia↗
PubMed1985

Displacing effects of chenodeoxycholic acid, ursodeoxycholic acid and sulfadimethoxine on plasma protein binding of tolbutamide.

The interactions between chenodeoxycholic acid (CDCA) or ursodeoxycholic acid (UDCA) and tolbutamide including its displacement from plasma protein binding sites were investigated pharmacokinetically. An increasing concentration of unbound tolbutamide was observed in the in vitro experiment, conducted by equilibrium dialysis method at 30 degrees C after the addition of CDCA and UDCA to human serum albumin (HSA), bovine serum albumin (BSA) and rabbit plasma containing tolbutamide. Small changes in total plasma concentration of tolbutamide were noted after high dose (0.167 mg/kg/min) intravenous infusion of CDCA to rabbits receiving a constant intravenous infusion of tolbutamide, but, such an observation was not obtained with low dose (0.083 mg/kg/min) of CDCA or with either high or low dose of UDCA. These results seem to indicate the displacement of high doses of CDCA. The coadministration of sulfadimethoxine which not only displaces tolbutamide from binding sites but also inhibits its metabolism was investigated. A different plasma pattern was obtained under the same intravenous infusion conditions, as compared with the plasma pattern resulting from tolbutamide-CDCA or UDCA combination.

Animals↗
PubMed1981

Bile acid composition affecting cholesterol dissolution rate: a use of multiple regression analysis.

The dissolution rate of cholesterol in human gallbladder bile was measured by a rotating-disk method using 14C-labeled cholesterol, and was compared with concentrations of the biliary lipids. Computed multiple regression analysis of the results showed that the dissolution rate of cholesterol could be presented as a function of the concentrations of deoxycholic and chenodeoxycholic acid (multiple correlation 0.905; F-value 51.8 (p less than 0.001)). To examine the effect of different kinds of bile acids on cholesterol solubilization, the cholesterol solubility in a gallbladder bile with addition of a conjugated bile acid was determined. Greater solubilization of cholesterol was observed in the bile with addition of sodium deoxycholylglycine and chenodeoxycholylglycine than that with addition of sodium cholylglycine. There was no additional enhancement of the solubility with addition of sodium ursodeoxycholylglycine. These results suggest that the cholelitholytic effect of chenodeoxycholic acid may be greater than that of ursodeoxycholic acid, since the administration of chenodeoxycholic or ursodeoxycholic acid to patients with cholesterol gallstones induced different alterations of biliary bile acid composition.

Bile Acids and Salts↗
PubMed1981

Factors affecting the cholesterol dissolution ability of human bile.

Bile samples were obtained from 13 patients with cholesterol gallstones at laparotomy. Control bile samples were obtained from 15 patients with gastric cancer or gastric ulcer. One mixed stone was cut in half and serial thin sections, 10 micrometers in thickness, were prepared from the cut surface. The solubility of cholesterol in these gallstone sections after immersion in the bile samples was observed microscopically after 1, 3, 5 and 24 hr. Of 15 control bile samples, 9 showed a marked cholesterol dissolution after 1 hr, and 6 showed it after 3 and 5 hr. Three out of 13 bile samples from the patients with cholesterol stones dissolved the gallstone section after 1 hr, and 7 after 3 and 5 hr. The dissolution was not observed in the remaining 3 bile samples. Cholesterol and total bile acid concentrations of the control bile were significantly higher than those of the bile from the cholesterol gallstone patients (p less than 0.05 and p less than 0.02, respectively). Correlative studies of the composition of bile and its ability to dissolve cholesterol revealed that bile samples with a high total bile acid concentration possessed a higher dissolution ability, even when the ratios of total bile acid to cholesterol were almost the same in control and cholesterol gallstone bile. On the basis of these findings, it may be concluded that the solubility of cholesterol in bile cannot simply be explained in terms of relative concentrations of cholesterol, phospholipids and total bile acid, because the absolute concentration of total bile acid also plays a significant role for the dissolution ability.

Bile↗
PubMed1976

Metabolism of chenodeoxycholic acid in hamsters.

The study on the metabolism after oral administration of chenodeoxycholic acid-24-14C was performed by analysis of radioactivity that had appeared in bile and feces of male hamsters. The radioactive bile acids were analyzed by thin layer chromatography and identified by the isotope dilution method. In the bile of the hamsters with bile fistula, radioactivity was originated from unchanged chenodeoxycholic acid for the most part, and 7-ketolithocholic acid, lithocholic acid, and beta-muricholic acid for the remainder. In the feces lithocholic acid, dehydrolithocholic acid, isolithocholic acid, and unchanged form were identified. After the multiple dosing of chenodeoxycholic acid-24-14C for 6 days, beta-muricholic acid was also identified in the feces.

Administration, Oral↗