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Biomedical subjects

T Satake

Publications and source records attributed to T Satake.

At least 217 records · Page 12Linked to original sources

Plasma concentrations of 6-keto-prostaglandin F1 alpha, thromboxane B2 and platelet aggregation in patients with essential hypertension.

Plasma concentrations of 6-keto-prostaglandin F1 alpha (6-keto-PGF1 alpha) and thromboxane B2 (TXB2), the stable nonenzymatic metabolites of prostacyclin and TXA2, respectively, were assayed in 26 patients with essential hypertension and 25 normotensive subjects to investigate the pathophysiological role of prostacyclin and thromboxane A2 (TXA2) in essential hypertension. A tourniquet test was also performed on the upper limb of each subject to study the reactivity in peripheral vessels. In addition, platelet aggregation was investigated. There were significantly increased plasma TXB2 concentrations and platelet aggregation and significantly decreased plasma 6-keto-PGF1 alpha concentrations in patients with essential hypertension as compared with normotensive subjects. The responses to tourniquet tests were also different. There were significantly increased plasma concentrations of 6-keto-PGF1 alpha and TXB2 and platelet aggregation in normotensive subjects, but no significant changes with essential hypertension as compared to resting values. These results indicate that the reduction of plasma prostacyclin and increase of plasma TXA2 may contribute to the maintenance of blood pressure elevation in patients with essential hypertension. In addition, it is also suggested that increased prostacyclin generation in normotensive subjects during the tourniquet test is a protective mechanism. In patients with essential hypertension, the protective activity is reduced.

6-Ketoprostaglandin F1 alpha↗

Phospholipid methylation in canine cardiac membranes. Relations to beta-adrenergic receptors and digitalis receptors.

Phospholipid methylation of canine cardiac membranes was studied in vitro to determine its relationship to the regulation and function of beta-adrenergic and digitalis receptors. Cardiac membranes were prepared from the left ventricle of mongrel dogs. Phospholipid methylation was assayed by measuring [3H] methyl incorporation after incubation with methyl donor S-adenosyl-L-[methyl-3H] methione at 37 degrees C. The reaction of phospholipid methylation had an optimum pH around 9 and a linear time course of up to 60 min. The reaction was inhibited by the addition of S-adenosyl-L-homocysteine, a known antagonist of biological transmethylation. L-isoproterenol enhanced phospholipid methylation markedly, but ouabain had no effect. On the other hand, after phospholipid methylation in cardiac membranes was stimulated by pre-incubation with S-adenosyl-L-methionine for 60 min at 37 degrees C, [125I] iodohydroxybenzylpindolol binding to the membranes was increased. The number of the beta-adrenergic receptor binding sites (Bmax), calculated from Scatchard analysis in cardiac membranes of 3 dogs significantly increased. On the other hand, [3H] ouabain binding and Na+, K+, Mg2+-ATPase activity were not increased. The increase in [125I] iodohydroxybenzylpindolol binding was inhibited by the addition of S-adenosyl-L-homocysteine. These binding suggest that phospholipid methylation is closely related to beta-adrenergic receptors, but not digitalis receptors in cardiac membranes.

Animals↗

[Small dose of ARA-C in the treatment of an elderly patient with acute myeloblastic leukemia].

A 79 year old man with a history of myocardial infarction and cerebral infarction was admitted to our hospital in August, 1982. The hematological examination showed anemia and leukopenia (myeloblast 12%), and bone marrow aspiration confirmed the diagnosis of acute myeloblastic leukemia (FAB, M2). Because his general condition was poor, he was treated with small dose of Ara-C (10 mg/m2/12 hr, subcutaneous injections), obtaining complete remission. In cases of acute myeloblastic leukemia in elderly patients where other intensive treatments are contraindicated, it appears to be useful to employ a method of small dose of Ara-C therapy.

Aged↗

[Bronchial asthma].

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Airway Obstruction↗