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66 巻, 5 号
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百々 修司, 宮崎 青爾, 坂中 昭典, 五井 麗司, 地守 研三, 三浦 清1990 年 66 巻 5 号 p. 529-542
発行日: 1990/05/20
公開日: 2012/09/24
ジャーナル フリーIn our present studies, we evaluated the role of the submandibular glands (SMG) on plasma inactive renin (PIR) releasing mechanisms in rats using some agents which are known to stimulate plasma active renin (PAR) release.
The results were analyzed between sialoadenectomized (SX) and sham-operated (control: C) rats. Twenty-four h after the operation, PAR releasing agents, furosemide (FRO) 2.5mg/rat/h with prior iv bolus 5mg, captopril (CAP) 5mg/rat/h with prior iv bolus 10mg, 1-Sar-8-Ile-angiotensin II (Ang II A) 300ng/kg/min, prostaglandin E1 (PGE1) 100ng/kg/min, and prostaglandin 12 (PGI2) 100ng/kg/min, were infused through femoral venous cannulae. Blood samples were taken through femoral arterial cannulae into test tubes containing 2mg EDTA-2Na. PAR was assayed by RIA, and total renin was obtained after tryptic activation. According to the responses of PIR, the agents used were categorized into three patterns: FRO increased PIR, both PGs lowered PIR, and, CAP and Ang II A had no effect on PIR release. The PIR release mechanisms by FRO were further investigated by 20mg FRO ip injection in totally nephrectomized rats. PIR increased even in nephrectomized rats, but the increase was totally canceled by the following SX. In conclusion, FRO alone among some agents studied is able to stimulate PIR release only under the existence of SMG.抄録全体を表示PDF形式でダウンロード (1267K) -
大澤 仲昭, 坂根 貞樹1990 年 66 巻 5 号 p. 543-556
発行日: 1990/05/20
公開日: 2012/09/24
ジャーナル フリーSwelling of the thyroid gland is a common symptom in patients with Graves' disease. However, until recently there were no adequate means of measuring the thyroid volume. In this study, thyroid volume (in Graves' disease patients on antithyroid drug (ATD) therapy) was measured serially by a new ultrasound technique involving the use of a specifically programmed computer. The relationships between thyroid volume and prognosis, and between thyroid volume and serum thyroglobulin (Tg) concentration were examined.
Sixty untreated patients with Graves' disease and 62 healthy subjects were included in the study. Twenty of the 60 patients with Graves' disease who had no anti-Tg antibodies underwent serial measurement of thyroid volume and serum Tg concentration during long term (18~42 months) ATD therapy.
Thyroid volume in normal subjects ranged from 5.6ml to 20.2ml, with a mean of 12.0±4.0ml. In patients with untreated Graves' disease, the volume ranged from 13.3 to 190.7ml with a mean of 40.2±27.8ml (n=60). Thyroid volume was significantly correlated with both serum Tg concentration (n=20, r=0.678, p<0.01) and serum TSH receptor antibody activity (n=18, r=0.590, p<0.01). During ATD therapy, the thyroid volume decreased gradually in most patients. Eleven of 20 treated patients experienced remission after therapy was discontinued, and in these patients, thyroid volume was significantly smaller (p<0.01) than before treatment. Four patients developed hypothyroidism due to over dosage of ATD at which time thyroid volume increased in all four. In the course of therapy, even during episodes of hypothyroidism changes in serum Tg concentrations paralleled changes in thyroid volume. After 12 months of therapy, thyroid volume expressed as a percentage of the pretreatment value was significantly smaller in patients in remission (77.6±8.9%) than in those who did not show remission (92.4±11.6%).
These data suggest that serial ultrasonographic measurement of thyroid volume is useful in predicting the course of hyperthyroidism in ATD-treated patients with Graves' disease.抄録全体を表示PDF形式でダウンロード (1719K) -
-ラットの摘出膵灌流による-武部 和夫, 川岸 隆彦1990 年 66 巻 5 号 p. 557-571
発行日: 1990/05/20
公開日: 2012/09/24
ジャーナル フリーTo examine the effects of growth hormone-releasing factor (GRF) on islet hormone release, rat pancreas was perfused. rhGRF at the concentration of 10-7M or more enhanced insulin secretion stimulated by 16.7mM glucose, hpGRF slightly enhanced insulin secretion as well. The insulin secretion induced by 10-6M rhGRF was completely inhibited by 10-6M propranolol. rhGRF at the concentration of 10-8M or more stimulated glucagon secretion even in the presence of 16.7mM glucose. The glucagon secretion stimulated by 10-6M rhGRF was inhibited in the early period but increased thereafter by 10-6M propranolol. 10-6M rhGRF slightly stimulated glucagon secretion in the presence of 16.7mM glucose when STZ diabetic rat pancreas was perfused. rhGRF at the concentration of 10-6M enhanced somatostatin secretion stimulated with 16.7mM glucose.
We concluded that rhGRF stimulated insulin, glucagon and somatostatin secretion and the insulin secretion was inhibited by β-blocker. hpGRF stimulated insulin and glucagon secretion as well.抄録全体を表示PDF形式でダウンロード (1297K) -
-IRMA法とRIA法との比較-熊本 悦明, 伊藤 直樹, 丸田 浩, 高木 良雄, 三熊 直人, 南部 明民, 立木 仁, 黒畑 敏江1990 年 66 巻 5 号 p. 572-583
発行日: 1990/05/20
公開日: 2012/09/24
ジャーナル フリーTo determine the normal range of serum LH and FSH levels, blood samples from 53 normal adult males were measured by a double antibody radioimmunoassay system and a new immunoradiometric assay (IRMA) system. It was necessary to evaluate the individual pulsatile secretion and the differences in measured values among laboratories to determine the normal range. Therefore, in 53 normal adult males lacking any evidence of hormonal abnormalities, blood was sampled at 9:00 a.m. daily for 3 days, and these samples were measured in 3 laboratories.
The result of the hormone concentration of blood sample was not appropriate as the normal range because of the high amplitude of LH and FSH pulses. Coefficient values (CV) between the mean value of the first two samples and the mean value of all three samples were small. Therefore, the mean value of the first two samples was clinically accurate for use as the normal range. Significant differences in measured values were observed among the 3 laboratories. The normal range, which included individual pulsatile secretion, and the differences in measured values among the laboratories was as followings: LH (RIA): 7.6-13.7mIU/ml, LH (IRMA): 2.1-4.7mIU/ml, FSH (RIA): 4.7-9.5mIU/ml, FSH (IRMA): 3.0-7.4mIU/ml.
The serum LH and FSH levels of 68 untreated male infertility patients tended to rate high with respect to our normal range. It was considered that the normal range determined in this study was useful for clinical management.抄録全体を表示PDF形式でダウンロード (987K) -
小島 元子, 佐藤 宏治, 五味渕 大平, 伊藤 信雄, 金 真治, 福地 総逸, 宮地 幸隆1990 年 66 巻 5 号 p. 584-596
発行日: 1990/05/20
公開日: 2012/09/24
ジャーナル フリーThis experiment was carried out to investigate the inhibitory effects of glycyrrhizin and its aglycon, glycyrrhetinic acid, on the metabolism of cortisol and prednisolone in vivo and in vitro.
The effects of glycyrrhetinic acid on the metabolism of cortisol were examined in vitro using rat and bovine liver homogenate. Glycyrrhetinic acid inhibits both hepatic Δ4-5-reductase and 11 β-hydroxysteroid dehydrogenase in a dose-dependent manner, resulting in the decrease of conversion of cortisol to cortisone, dihydrocortisol and tetrahydrocortisol in rats. The concentrations of glycyrrhetinic acid inducing 50%inhibition of rat liver Δ4-5-reductase and 11 β-hydroxysteroid dehydrogenase were 2.5×10-6M and 8.5×10-6M, respectively. Glycyrrhetinic acid also inhibits bovine liver 11 β-hydroxysteroid dehydro-genase and 20-hydroxysteroid dehydrogenase in a dose-dependent manner, resulting in the decrease of conversion of coritsol to dihydrocortisol and prednisolone to 20-dihydro-prednisolons. The concentrations of this drug inducing 50%inhibition of 11 β-hydroxysteroid dehydrogenase and 20-hydroxysteroid dehydrogenase were 8.2×10-6M and 6.5×10-6M, respectively. This is the first report which demonstrates the marked inhibitory effects of glycyrrhetinic acid on 11 β-hydroxysteroid dehydrogenase and 20-hydroxysteroid dehydrogenase in vitro.
The effects of glycyrrhizin on the rate of metabolism of cortisol as well as prednisolone were studied in 23 patients with or without adrenal insufficiency. Glycyrrhizin had no effect on diurnal rhythm of plasma cortisol in 7 control subjects with normal pituitary adrenal axis, whereas glycyrrhizin significantly increased the half-time (T1/2) and area under the curve (AUC) for plasma cortisol in 4 patients with adrenocortical insufficiency taking oral cortisol. Glycyrrhizin also increased T1/2 and AUC for plasma prednisolone in 12 patients taking an oral prednisolone for at least 3 months. These results indicate that the suppression of hepatic Δ4-5-reductase, 11 β-hydroxysteroid dehydrogenase and 20-hydroxysteroid dehydrogenase by glycyrrhizin and glycyrrhetinic acid may delay the clearance of cortisol and prednisolone and prolong the biological half-life of cortisol or prednisolone.抄録全体を表示PDF形式でダウンロード (1094K)
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