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Biomedical subjects

S Ohtake

Publications and source records attributed to S Ohtake.

At least 199 records · Page 11Linked to original sources
PubMed1982

Induction of antitumor immunity by tumor cells treated with abrin.

Abrin is known as a cytotoxic lectin. Immunization with Meth-A tumor cells which were treated in vitro with abrin induced a strong antitumor immunity in syngeneic BALB/c mice. The immunizing effect was stronger than that produced by an irradiated Meth-A tumor cell vaccine. Studies on the mechanisms of the immunizing effect with the abrin-treated tumor cells demonstrated that abrin acts as an immunoadjuvant. Furthermore, the regression of a growing Meth-A tumor was observed after abrin was injected into the tumor, while the induction of a strong antitumor immunity also occurred. It appears, therefore, that the antitumor effects of abrin are attributable to two kinds of activity: cytotoxicity and adjuvant activity.

Abrin↗
PubMed1980

A simple rapid autoradiography for 3H-thymidine labeling index and its application to therapy of adult acute leukemia.

Our simple rapid autoradiography for 3H-thymidine (3H-TdR) labeling index (LI) of leukemic cells was introduced. Thirty-nine adult patients with acute nonlymphocytic leukemia were treated under a new protocol using 3H-TdR LI as a parameter and inserting a trial of partial synchronization by Ara-C. The success rate of synchronization by Ara-C (rise of the LI up to 10%) was 62.5% out of 32 courses. By our regimen the complete remission (CR) rate of 71.4% in 35 first treated cases, that of 44.0% in 25 courses of recurrent cases, and a median survival of 12 months were achieved. A survey of literature revealed that our results were favorably compared with others. Our new protocol is advantageous in permitting one to precisely know the proper time for chemotherapy and thus avoiding unnecessary side effects.

Acute Disease↗
PubMed1979

Antihypertensive action of d,l-alpha-tocopheryl nicotinate in rats.

The effects of d,l-alpha-tocopheryl nicotinate (EN) on model hypertension in rats were studied in comparison with d,l-alpha-tocopheryl acetate (EA). The progress of hypertension in young SHR during the 9th to 15th weeks after birth was markedly accelerated by replacing their driking water with 1% saline. The highly-developed hypertension in old SHR (9 months of age) was further advanced by salt-loading. Oral administration of 20 or 100 mg/kg of EN or 88 mg/kg of EA, once a day, delayed the progress of hypertension in young SHR and reduced advanced hypertension in old SHR. An antihypertensive effect of tocopheryl esters was also found in DOCA-salt hypertensive rats. The treatment with EN or EA definitely reduced the incidence of pathological changes accompanying model hypertension such as suppressed weight gain, pulmonary edema, myocardial fibrosis, cerebral hemorrhage and protected the animals from death. In antihypertensive effect, EN was about 5 times more active than EA in molecular base, and the effects of EN protecting from pathological changes associated with model hypertension were more definite than those of EA. The treatment with EN or EA reduced water and sodium retention in the DOCA-salt hypertensive animals. This fact may suggest the implication of a mechanism through electrolyte metabolism in the antihypertensive action of these tocopheryl esters.

Animals↗
PubMed1978

Chronic hypertension induced by streptozotocin in rats.

An intravenous injection of 40 or 65 mg/kg streptozotocin induced not only diabetes but also severe hypertension in rats. Whereas the hyperglycemia developed fully within a few days after the injection of streptozotocin, the hypertension progessively advanced and reached maximum level several weeks after the treatment and lasted more than 20 weeks. Twenty mg/kg streptozotocin did not induce hyperglycemia but significantly increased blood pressure several weeks after the treatment. Arrest of growth, polyuria, glycosuria, hyperlipemia and lenticular cataracts developed in the animals treated with 40 or 65 mg/kg streptozotocin, but in none of the animals treated with 20 mg/kg. In histological examinations in the 24th week after the treatment, degranulation and necrosis in the pancreatic beta-cells, and vacuolization and deposition of PAS-positive materials in the renal proximal tubules were found in the animals treated with 40 or 65 mg/kg streptozotocin.

Animals↗
PubMed1978

A new method for extraction of extravasated dye in the skin and the influence of fasting stress on passive cutaneous anaphylaxis in guinea pigs and rats.

A method for quantitative extraction of extravasated dye from the skin was studied in guinea pigs and rats. A simple method with a low cost and good recovery was established as follows; A piece of the skin containing extravasated dye was soaked overnight in a stoppered glass tube containing 1 ml of 1 N KOH at 37 C. Then, 9 ml of mixed solution of 0.6 N H3PO4 and acetone (5:13) was added to the tube. The tube was shaken vigorously for a few seconds and centrifuged at 3,000 rpm for 15 min. Absorbance of supernatant was measured at 620 nm. The recovery rate of the dye was about 95 per cent both in guinea pigs and rats. Using this method we observed that fasting stress significantly reduced the intensity of skin reaction induced by chemical mediators, heterologous PCA and especially homologous PCA in guinea pigs.

Acetone↗
PubMed1977

Antihypertensive effect of combined treatment with alpha- and beta-adrenergic blockers in the spontaneously hypertensive rat.

Using a continuous systolic monitor, effects of oral administration of three alpha-adrenergic blockers, i.e. phenoxybenzamine, phentolamine and a new quinazoline compound (2-[4-(n-butyryl)-homopiperazine-1-yl]-4-amino-6, 7-dimethoxy-quinazoline; E-643), on blood pressure and heart rate in normotensive Wistar rats (NWR) and spontaneously hypertensive rats (SHR). 1) An oral dose of 1 mg/kg phenoxybenzamine or E-643 almost completely reversed pressor response to adrenaline (2 microgram/kg i.v). Phentolamine was 3 to 5 times less effective than phenoxybenzamine and E-643. These alpha-blockers reduced pressor response to noradrenaline (2 microgram/kg i.v.) merely to one half at an oral dose of 100 mg/kg. 2) All these alpha-blockers did not reduce blood pressure but markedly increased heart rate in NWR. On the other hand, they reduced blood pressure of SHR without marked increase in heart rate. Although the alpha-blocking and cardiac stimulating effects of phenoxybenzamine lasted more than several days, its hypotensive effect in SHR disappeared within 24 hours. 3) An oral dose of 30 mg/kg propranolol did not reduce blood pressure in both NWR and SHR but slightly decreased heart rate. The combined treatment of these alpha-blockers with propranolol completely abolished the cardiac stimulating effect of the alpha-blockers and resulted in a definite reduction in blood pressure of NWR and potentiated the hypotensive effect of alpha-blockers in SHR.

Administration, Oral↗
PubMed1976

Anti-hypertensive action of DL-alpha-tocopharyl esters in rats.

1. Oral administration of DL-alpha-tocopheryl nicotinate (EN) (0-04 or 0-2 mmol day-1 kg-1) or DL-alpha-tocopharyl acetate (EA) (0-2 mmol day-1 kh-1) delayed the progress of hypertension in unilaterally nephrectomized rats, which were treated with deoxycorticosterone and salt, and in genetically hypertensive rats (SHR) which were given sodium chloride solution. Suppression of body weight gain, incidence of pneumonia and mortality were reduced by treatment with EN or EA. 2. Severe hypertension in old SHR (9 months) further progressed, when drinking water was replaced by sodium chloride solution, and four out of ten of these animals died of cerebral haemorrhage during 4 weeks. The administration of EN or EA prevented the increase in blood pressure and incidence of stroke.

Animals↗
PubMed1976

[Protective effect of tocopheryl esters on pulmonary edema induced by epinephrine].

The present study was performed in order to determine protective effect of dl-alpha-tocopheryl nictonate (EN) and dl-alpha-tocopheryl acetate (EA) on pulmonary edema induced by epinephrine (Epi) in mice. The tocopheryl esters were orally administered once a day for 10 days. Epi was then infused to induce pulmonary edema 3 hr after the final dosing. One or three min infusion of 0.01% Epi at a rate of 0.1 ml/min provoked toxic syndromes as pilorection, exophthalmos and salivation. Some animals died of respiratory failure. The lung weight either wet or dry increased after the EPi infusion and diffuse hemorrhage into alveoles was microscopically recognized in untreated animals. However, these findings were of lesser degree in animals receiving NE (20, 50 and 100 mg/kg/day) and Ea (corresponding doses with EN in molecular weight basis). When comparing the effect of EN with that of EA on the increase of lung weight and death from the Epi infusion, EN was more protective than EA. Although the mechanism of protecting action of these tocopheryl esters remains obscure, the interpretation is that these compounds did not affect the pressor response to Epi.

Animals↗