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Biomedical subjects

S Miyabo

Publications and source records attributed to S Miyabo.

At least 109 records · Page 6Linked to original sources
PubMed1984

OP-1206, a prostaglandin E1 derivative. Effects of oral administration to patients with chronic lung disease.

In order to assess the clinical effectiveness of an oral prostaglandin E1 derivative, OP-1206, five patients with chronic obstructive pulmonary disease and two with pulmonary fibrosis were studied from the standpoint of hemodynamics and nine others with chronic lung disease from the standpoint of respiratory function. Oral intake of OP-1206 resulted in a significant decrease in the pulmonary arterial pressure (p less than 0.01), total pulmonary vascular resistance (p less than 0.01), pulmonary arteriole resistance (p less than 0.01), and total systemic vascular resistance (p less than 0.05), and an increase in the cardiac index (p less than 0.05) and oxygen delivery (p less than 0.01) with insignificant changes of PaCO2, PaO2 and pH. There was no clinical improvement of lung function after OP-1206 intake. OP-1206 is a potent vasodilator, improving cardiac performance in patients with chronic lung disease and possibly preventing the progress of cor pulmonale in this kind of patient.

Aged↗
PubMed1984

Effects of 2-hydroxyoestradiol and 4-hydroxyoestradiol on gonadotrophin and prolactin secretion in women.

In order to investigate the effects of 2-hydroxyoestradiol (2-OHE2) and 4-hydroxyoestradiol (4-OHE2) on the release of human pituitary hormones, each steroid (500 micrograms single bolus) was injected to young women during the follicular phase. Both steroids resulted in a transient suppression followed by a small rise of LH and FSH. 4-OHE2 appeared to be more potent than 2-OHE2. Injection of only the vehicle caused no change in gonadotrophin levels. The morning fall of plasma Prl was common in young women as an expression of circadian variation. Although the Prl fall tended to be greater in the 4-OHE2 group, analyses failed to reach statistical significance.

Adult↗
PubMed1984

The effect of insulin-dextran complexes on the protein synthesis in the primary monolayer culture of adult rat hepatocytes.

The purpose of the present study was to investigate the mechanisms of the long-term effects of insulin on protein synthesis in rat liver parenchymal cells. Three kinds of soluble and stable insulin-dextran complexes (I: Mr 150,000; II: Mr 450,000; III: Mr 2,000,000) were prepared. The effects of insulin or insulin-dextran complexes on protein synthesis were evaluated in the primary monolayer culture of adult rat liver. To avoid the effects of serum factors, the primary monolayer culture of adult rat liver in serum free medium was established. The cultured hepatocytes well maintained the metabolic and morphological characteristics of the adult rat liver. The incorporation of [14C]-leucine into trichloroacetic acid insoluble proteins and immunoprecipitates by anti-rat albumin serum were measured in cultured hepatocytes prepared either from the control or streptozotocin-induced rats. An addition of insulin-dextran complexes to the culture medium of the hepatocytes from diabetic rats stimulated the protein synthesis as well as the native insulin. The maximal effect of insulin-dextran complex (I) on protein synthesis was comparable to native insulin. However, insulin-dextran complex (II) caused a 67% stimulation of native insulin. Insulin-dextran complexes (III) induced only a slight increase of protein synthesis. Furthermore, an addition of insulin-dextran complexes into the medium caused a more tight cellular attachment to the dish and more extensive spreading. These results favor the view that the stimulation by insulin of protein synthesis in rat hepatocytes does not require the entry of insulin into cells.

Albumins↗
PubMed1984

Plasma lipoproteins of monosodium glutamate-induced obese rats.

The plasma lipids and lipoproteins of rats developing obesity after neonatal administration of monosodium glutamate (MSG) were compared with those obtained from controls. The MSG-treated rats, in addition to being stunted and having enlarged adipose tissue stores, showed reduced body weight and food intake. These rats revealed a marked increase of plasma triglyceride and a slight but significant increase of phospholipids in both male and female. There was no significant difference in plasma cholesterol between MSG-treated rats and controls. The lipids and protein concentrations of very low density lipoprotein (VLDL: d less than 1.006 g/ml) were significantly greater in the MSG-treated rats than in the controls. There were no changes in the composition of these increased VLDL, which indicated that the number of VLDL particles was increased. Plasma triglyceride and lipids components of VLDL were significantly greater in males than in females. In spite of hypophagia, both male and female MSG-treated rats had higher plasma glucose levels than sex-matched controls. Plasma insulin level was higher in male MSG-treated rats (49.3 +/- 6.6 microU/ml [s.e.]) than in female MSG-treated rats (14.3 +/- 3.2 microU/ml) or in male control rats (34.6 +/- 6.6 microU/ml). These results suggested that hyperinsulinemia plays an important role in the increase of VLDL observed in the MSG-treated male rats.

Animals↗
PubMed1982

Effect of the catecholestrogen 2-hydroxyestradiol on the renin-angiotensin system in the rat.

The effects of the catecholestrogen 2-hydroxyestradiol (250 and 500 micrograms/day, each for 7 days) on plasma renin substrate (PRS), activity (PRA) and concentration (PRC) were studied in male rats as compared with those of estradiol (250 micrograms/day, for 7 days) and vehicle alone (for 7 days). Pre-treatment levels of PRS, PRA, PRC and the PRA/PRC ratio were similar in four groups. After vehicle treatment, PRS, PRA, PRC and the PRA/PRC ratio remained unchanged. Estradiol treatment, however, produced an increase in PRS, an increase in PRA but no change in PRC. The PRA/PRC ratio after estradiol treatment was high. On the other hand, 2-hydroxyestradiol treatment caused no increase in PRS at a daily dose of 250 micrograms and a slight but significant increase in PRS at a daily dose of 500 micrograms. This treatment also produced increases in PRA as well as PRC at the two daily doses. These increases in PRA and PRC tended to be higher at a daily dose of 500 micrograms than at a daily dose of 250 micrograms. The PRA/PRC ratios after 2-hydroxyestradiol treatment were unaltered at the two daily doses. It is concluded that, while 2-hydroxyestradiol is less active in increasing PRS than estradiol, the compound is capable of increasing PRC.

Angiotensinogen↗
PubMed1981

A comparison of the bioavailability and potency of dexamethasone phosphate and sulphate in man.

The metabolic fate and ACTH-suppressant activity of two injectable dexamethasone esters, 21-phosphate and 21-sulphate, were studied in healthy men. After i.v. injection of 20mg free steroid alcohol, dexamethasone phosphate was efficiently hydrolyzed to free dexamethasone, reaching its peak plasma concentration within 5 min. About 9% of the administered dose appeared in the urine as free dexamethasone. By contrast, virtually no free dexamethasone was found in plasma and urine after injection of dexamethasone sulphate. Pharmacokinetic analysis showed that dexamethasone sulphate had a shorter plasma half-life and a higher metabolic clearance rate than free dexamethasone. A larger fraction (60%) of dexamethasone sulphate was rapidly excreted unmetabolized in urine. The plasma cortisol level was significantly suppressed for more than 24h after dexamethasone phosphate, while the plasma cortisol profile after dexamethasone sulphate merely showed physiological circadian variations. When the steroid esters were injected after pretreatment with metyrapone, a definite suppression of plasma ACTH was noted after dexamethasone phosphate, but again, dexamethasone sulphate was ineffective. These results cast serious doubt on the clinical value of dexamethasone sulphate as an injectable glucocorticoid, and critical reevaluation of this preparation is needed.

Adrenocorticotropic Hormone↗