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Biomedical subjects

A Okamoto

Publications and source records attributed to A Okamoto.

At least 217 records · Page 12Linked to original sources
PubMed1981

Erythrocyte deformability improving action of beta-pyridylcarbinol tartrate.

beta-Pyridylcarbinol tartrate was found to prevent the hyperosmotically induced worsening of filterability of rat erythrocytes after in vivo treatments. The effect is attributed to the prevention of the morphological change of the erythrocytes from normal discocytes to echinocytes. The study was made using a scanning electron microscope.

Animals↗
PubMed1981

Changes of portal vein pressure and intrahepatic blood vessels after surgery for biliary atresia.

The portal vein pressure was measured and biopsies of the liver were taken during the corrective operation in 31 patients with biliary atresia and during relaparotomy in 16 patients free from jaundice 4 mo to 9 yr after a successful corrective operation. Because the portal vein pressure was higher than 200 mmH2O in about 70% of patients during the corrective operation, portal hypertension appears to have already developed in most of the patients with biliary atresia at 2-4 mo of age. In the patients who had had frequent episodes of postoperative cholangitis, the portal vein pressure was elevated and the amount of interstitial tissue in the liver was markedly increased at reoperation compared with those at the corrective operation. These results showed that postoperative cholangitis aggravated portal hypertension and fibrosis of the liver. On the contrary, the portal vein pressure declined in patients in whom active bile drainage had persisted and cholangitis had not been complicated after operation. An early corrective operation and prevention of postoperative cholangitis are of the greatest important for prevention of development of the portal hypertension and cirrhosis of the liver in long-term survivors after surgery for biliary atresia.

Bile Ducts↗
PubMed1978

Adrenal hypertrophy produced by 17alpha-esterified glucocorticoids in rat foetus.

Glucocorticoids were injected sc into rat foetuses through the uterine wall on day 19 of intrauterine development; two days later the foetuses were removed and their adrenal glands were weighed. Some betamethasone derivatives produced marked adrenal hypertrophy in the foetuses. Structural characteristics of the effective compounds were 17alpha-esterification and 16beta-methylation. 9alpha-Halogenation and 21-esterification of glucocorticoids were not essential for producing the hypertrophy. Propionic acid at the C-17 position was more effective than valeric and acetic acids in producing the hypertrophy. The effect of betamethasone 17, 21-dipropionate was dose-responsive and prevented by simultaneous administration of betamethasone 21-disodium phosphate. Results obtained with decapitated or encephalectomized foetuses suggested that the hypertrophy produced was not due to a direct action of the glucocorticoids on the adrenal gland, but mediated by the hypothalamo-pituitary system.

Adrenal Gland Diseases↗