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Biomedical subjects

K Ohtake

Publications and source records attributed to K Ohtake.

72 records · Page 4Linked to original sources
PubMed1987

Calcium hopantenate, a GABA agonist, induces elevation of plasma beta-endorphin-like immunoreactivity levels in rats.

The effects of calcium hopantenate (HOPA) on plasma beta-endorphin-like immunoreactivity (beta-En-LI) levels in rats have been studied. HOPA (1.5 g/kg) was injected ip, and the animals were serially decapitated. The plasma beta-En-LI levels were measured by radioimmunoassay. Effects of HOPA on beta-En-LI release from the anterior pituitary were also investigated by means of an in vitro experiment. The beta-En-LI content in the hypothalamus and pituitary gland did not change significantly after HOPA injection. The plasma beta-En-LI levels increased significantly in a dose-related manner with a zenith at 30 min after HOPA injection. Effects of HOPA on plasma beta-En-LI levels were prevented with the pretreatment of bicuculline. The beta-En-LI release from the anterior pituitary was enhanced with the addition of HOPA to the medium, and HOPA's effects were blocked with an addition of bicuculline to the medium. These findings suggest that HOPA acts on the anterior pituitary to stimulate beta-En-LI release, and its effects are mediated via GABA receptor.

Animals↗
PubMed1983

[Autopsy case of adult T cell leukemia associated with hypertrophy of the parathyroid glands].

An autopsy case of adult T cell leukemia associated with hypercalcemia and hyperplastic parathyroid glands is reported. A 51-year-old man complained of systemic lymphadenopathy and hepato-splenomegaly; a diagnosis of adult T cell leukemia was made based on clinico-pathological findings. The pathogenesis of hypercalcemia in adult T cell leukemia is discussed. However, cases associated with hyperplasia of the parathyroid gland are very rare. We emphasize the role of the parathyroid gland in the pathogenesis of hypercalcemia in adult T cell leukemia.

Cell Division↗
PubMed1979

PaCO2 for optimum washout of inhalational anesthetics from the brain. A model study.

A hypothesis was established that, during emergence of inhalational anesthesia, hyperventilation and accompanying hypocapnia beyond a certain limit may actually disturb rather than enhance the washout of inhalational anesthetics from the brain because of a decreased cerebral blood flow. Two mathematical models were constructed and the washout of nitrous oxide, halothane and methoxyflurane were studied. In model I, the whole body consisted of a single compartment, and blood flow to this compartment was assumed to change proprotionally with the PaCO2. In model 2, the body was divided into two compartments, brain and the rest of the body. It was assumed that the blood flow to the brain compartment varies proportionally with the PaCO2, while that to the rest of the body remains constant. The analysis indicated that there indeed existed the PaCO2 values at which the washout of anesthetics from the brain can be maximally achieved. In model 1, they were 49.0, 22.1 and 9.7 mmHg for nitrous oxide, halothane, and methoxyflurane, respectively. In model 2, these PaCO2 values varied with time. While the hypothesis was proven to be valid, we conclude that it is of limited clinical significance. For halothane and methoxyflurane, these theoretically optimum PaCO2 values are sufficiently low. For nitrous oxide, the variation of PaCO2 makes little difference clinically, because its washout is fast enough regardless of PaCO2.

Anesthesia, Inhalation↗
PubMedDate not supplied

Effects of histamine and related compounds on the release of immunoreactive thyrotropin-releasing hormone from the rat stomach in vitro.

Effects of histamine and related compounds on the release of immunoreactive thyrotropin-releasing hormone (ir-TRH) from the rat stomach in vitro were studied. The rat stomach was incubated in medium 199 with 1.0 mg/ml of bacitracin and 100 micrograms/ml of ascorbic acid (pH 7.4) for 20 min. The amount of TRH release into the medium was measured by radioimmunoassay. The ir-TRH release from the rat stomach was enhanced significantly in a dose-related manner with the addition of histamine and inhibited with the addition of famotidine, but not with mepyramine. The stimulatory effect of histamine on ir-TRH release from the stomach was partially blocked with the addition of famotidine, but not with mepyramine. The elution profile of acid-methanol-extracted rat stomach on Sephadex G-10 was identical to that of synthetic TRH. These findings suggest that histamine stimulated ir-TRH release from the rat stomach in vitro, and that histamine's effects may be mediated via a H2-receptor.

Animals↗