日本内分泌学会雑誌
Online ISSN : 2186-506X
Print ISSN : 0029-0661
ISSN-L : 0029-0661
62 巻, 2 号
選択された号の論文の7件中1~7を表示しています
  • 武田 仁勇, 宮森 勇, 池田 正寿, 越田 英夫, 岡本 清也, 安原 修一郎, 森瀬 敏夫, 川東 正範, 竹田 亮祐
    1986 年 62 巻 2 号 p. 61-68
    発行日: 1986/02/20
    公開日: 2012/09/24
    ジャーナル フリー
    The present investigation was undertaken to elucidate the possible interplay between the circulating kinin (s) and the renin angiotensin axis in hyperthyroidism.
    The responsiveness of plasma aldosterone (p-Ald), kinin (p-BK), plasma renin activity (PRA) and serum angiotensin converting enzyme activity (ACEA) to infusion of angiotensin II at a dose of 4, 8 and 16 ng/kg.min. was asessed in 15 hyperthyroid pateints and 10 euthyroid controls. There was impaired angiotensin II induced response of blood pressure in hyper-thyroid pateints, and basal concentrations of p-Ald were 7.7±3.8 ng/dl in euthyroid controls and 12.6±3.1 ng/dl in hyperthyroid patients (p<0.05).
    As compared to the euthyroid controls, the hyperthyroid patients showed a reduced response of plasma aldosterone to angiotensin II infusion. Angiotensin II infusion increased p-BK from basal levels of 19.1±8.2 pg/ml to 31.0±7.8 pg/ml (p<0.05) only in hyperthyroid patients and did not increase ACEA in either group.
    Next, the effects of a single administration of captopril (50 mg p.o.) on blood pressure and p-BK in hyperthyroid patients and euthyroid controls were studied. In the two groups blood pressure was not changed by captopril, but p-BK increased significantly.
    The present results do not support the view that there may be a direct linkage between the kallikrein kinin system and the renin angiotensin axis mediated by kininase II or angiotensin converting enzyme in human peripheral blood. Also it is unlikely that kinin may play a role in the mechanism of reduced responsiveness of aldosterone and blood pressure to angiotensin II in hyperthyroidism.
  • 古村 正
    1986 年 62 巻 2 号 p. 69-81
    発行日: 1986/02/20
    公開日: 2012/09/24
    ジャーナル フリー
    It is well known that serum calcitonin (CT) levels in infantile rats are higher than those in adult rats. In the present experiment, the effects of parathyroidectomy or calcium administration on serum calcitonin levels were observed in suckling rats.
    Bilateral parathyroidectomy (Px) on 3-, 5-, 7-, 8- or 14-day-old Wistar-Imamichi female rats was performed surgically under a dissecting microscope. Ether anesthesia was used. In the first experiment, the Px rats of various age groups were killed 1 week after the operation. In the second experiment, time course effects of Px on one-week-old rats were observed 1, 2 or 3 weeks after the operation. CT in the serum and thyroid extracts (0.001N HC1) was measured using radioimmunoassay kits for human CT. Serum Ca was measured by the OCPC method and serum inorganic phosphates was measured by the Takahashi method.
    Serum calcium levels showed a significant decrease 1 week after Px in all age groups. In these rats, serum CT levels showed a slight increase or no changes, and a significant increase in CT concentrations in the thyroid gland was observed in all age groups. Moreover, the increase in CT contents in the thyroid gland became larger 3 weeks after Px in rats operated on at one week of age. Thyroid extract containing 70 pg immunoreactive CT was effective in decreasing 1.22 mg/100 ml serum calcium at 15 min after i.v. injection in a bioassay system in which a dose response curve of human calcitonin was used as standards. Acute s.c. injection of CaCl2 solution resulted in a significant increase in serum CT levels 15 and 30 min later in intact 2- and 3-week-old rats, whereas no significant change in serum CT levels was observed in one-week-old intact rats. Three and 15 min after s.c. injection of Na2 EDTA, serum Ca levels decreased markedly, but thyroidal CT contents tended to increase 3 and 5 min after the injection.
    The results indicated that parathyroidectomy in infantile rats induces a marked increase in biologically active calcitonin in the thyroid gland, inspite of the significant decrease of serum Ca levels.
  • 清水 隆之, 井上 和子
    1986 年 62 巻 2 号 p. 82-96
    発行日: 1986/02/20
    公開日: 2012/09/24
    ジャーナル フリー
    Synthetic human pancreatic growth hormone-releasing factor (hpGRF-44) was given by i.v. bolus injection to 15 normal non-obese and 32 obese subjects who were divided into two groups according to their ages-group A : young subjects, 20-50 yrs., and group B : old subjects, more than 60 yrs. In normal subjects, hpGRF-44 had no effect on the secretion of PRL, TSH, LH, FSH, IRI and cortisol. hpGRF-44 stimulated GH secretion selectively. However, the serum GH responses were different between the young and old groups, the peak GH levels being significantly higher in the young group than in the old group (20.1±4.2 vs. 7.5±1.6 ng/ml; group A vs. B; p<0.05). At the doses of 0.5, 1.0, 2.0 and 4.0 μg/kg B.W., the serum GH responses were similar in an individual subject.
    In young obese subjects, the peak GH levels to hgGRF-44, 1.0 μg/kg B.W. were significantly lower than those in young normal subjects (4.3±0.6 vs. 20.1±4.2 ng/ml; obese vs. normal; p<0.01). In old subjects, the peak GH levels to hpGRF-44, 1.0 μg/kg B.W. were similarly diminished in both normal and obese subjects. However, the integrated response of GH was significantly lower in obese subjects than in normal subjects (405.9±58.7 vs. 755.9±134.2 ng·min/ml; obese vs. normal; p<0.05).
    In 5 young obese subjects, regular insulin (RI) injection (0.15 U/kg B.W.) and arginine drip infusion (0.5 g/kg B.W.) alone, and simultaneous injection of hpGRF-44, 1.0 μg/kg B.W. and RI, 0.15 U/kg B.W. were done. In these subjects, GH responses to RI or arginine infusion were diminished as in the case of hpGRF-44 administration, whereas the peak GH levels were higher in the RI stimulation. The combination of hpGRF-44 and RI partially restored GH response. (peak GH levels; 14.6±0.8 ng/ml).
    These results confirm the age difference of serum GH response to hpGRF-44 and also indicate that obese subjects show low or no response to hpGRF-44 administration. The fact that insulin hypoglycemia induced larger serum GH response than hpGRF-44 in obese subjects may suggest the existence of GH-releasing substances other than hpGRF-44.
  • 三木 京子
    1986 年 62 巻 2 号 p. 97-107
    発行日: 1986/02/20
    公開日: 2012/09/24
    ジャーナル フリー
    A new method for determining thyroid gland volume was developed by means of computerized ultrasonography. A maximum area of the thyroid (S) was obtained from coronal sections and a maximum thickness (C) was obtained from sagittal sections. The thyroid volume was then calculated by SXC. The volume of phantoms and pig thyroids obtained by this method was identical with the actual volume. The thyroid volume in this method correlated well with the estimated volume in patients with Graves' disease undergoing thyroidectomy (r=0.954). The measurement was then performed in 56 healthy subjects (male 28, female 28, age 15' 68 y.o.) and 126 patients with thyroid diseases.
    The thyroid volume in healthy men was significantly larger than that in women (18.4±6.1ml vs 13.9±4.9ml, Mean±SD, p<0.01). The thyroid volume in normal subjects correlated with body height, body weight or body surface area (p<0.01), which may explain the sex differences.
    An attempt was made to calculate the prospective thyroid volume (Y ml) from body height as follows;
    Y = 0.425×- 52.8, X; body height (cm).
    Four out of thirty patients with untreated Graves' disease had a gland volume of the normal range, but in all patients the thyroid volume was larger than the prospective volume. The thyroid volume and the rate of volume increase (determined thyroid volume/calculated prospective volume) were correlated with the serum levels of T3 T4 concentration in the untreated stage. The volume and the rate of volume increase did not correlate with serum TSH receptor antibody activity.
    The thyroid volume in patients with Graves' disease who had been in remission (33.0±13.5 ml) was significantly smaller than that in untreated patients (51.8±24.4 ml, p<0.02).
    These findings indicate that the present method is reliable and clinically useful for the investigation of thyroid diseases.
  • 西井 修, 竹内 亨, 高橋 稔, 岡村 隆, 柳沼 〓, 小林 拓郎
    1986 年 62 巻 2 号 p. 108-116
    発行日: 1986/02/20
    公開日: 2012/09/24
    ジャーナル フリー
    Eight women with normal term pregnancy were i.v. administered 10 mg Metoclopramide (M), dopamine antagonist, before and during labor. Serum prolactin (PRL), TSH, GH and cortisol levels were measured at -30, 0, 30 and 60 minutes after M administration by specific radioimmunoassay. Basal serum PRL levels before labor, 287.5±28.6 ng/ml (mean±S.E.), significantly declined during labor to 237.0±22.4 and 216.4±22.9 ng/ml (p<0.05 at both) at 0 and 30 minutes before M administration, respectively. The increments in serum PRL at 30 and 60 minutes after M administration during labor (209.5±33.9 and 120.0±27.1 ng/ml, respectively) were not significantly different from those before labor (202.1±48.7 and 89.9±30.1 ng/ml, respectively), suggesting that the decline in serum PRL levels during labor is not due to the dopaminergic control. Basal serum TSH and GH levels were not significantly changed by labor and M administration either before or during labor. Serum cortisol levels tended to increase during labor, but these changes were not significant. The data suggest that the PRL releases from the pituitary during labor are not controlled by the dopaminergic mechanism.
  • 合阪 幸三, 安藤 三郎, 國保 健太郎, 吉田 浩介, 森 宏之
    1986 年 62 巻 2 号 p. 117-125
    発行日: 1986/02/20
    公開日: 2012/09/24
    ジャーナル フリー
    It is well known that the luteal function in the patients with hyperprolactinemia is much suppressed by high level of serum prolactin. Present study was performed to investigate whether the luteal function in the patients with transient or occulted hyperprolactinemia was affected by the transient increase of serum prolactin level.
    The circadian changes of serum FSH, LH, prolactin, estrone, estradiol and progesterone levels were examined in seven cases of the transient or occulted hyperprolactinemia whose BBT charts showed biphasic patterns. Serum prolactin levels of these patients were less than 25 ng/ml at daytime and more than 150 ng/ml at 30 minutes after the administration of 500 μg of TRH. Blood samplings were taken every two hours through an intravenous indwelling catheter without any disturbances. All of the patients had their breakfast at 7 to 8, lunch at 11 to 12 and dinner at 17 to 18 o'clock and slept from 22 until 6 in the next morning. Serum FSH, LH, prolactin, estrone, estradiol and progesterone levels were determined by RIA and the circadian changes of these hormones were analysed. Then, 5 mg of bromocriptine was administered every day to these patients for more than 30 days and the duration of the luteal phase and the mid-luteal serum estradiol and progesterone levels for the indicators of the luteal function were examined before and after the administration of bromocriptine.
    The circadian changes of serum prolactin levels in the patients showed significant increase during both daytime and night compared to those of the control (p<0.005, p<0.005). Moreover, serum prolactin levels of the patients during night also showed significant increase compared to those during daytime (p<0.005). There was no conspicuous change in the circadian profiles of serum FSH, LH, estrone and estradiol levels. However, the circadian profile of serum progesterone levels showed significant decrease during night in the patients with transient or occulted hyperprolactinemia, and the significant negative correlation could be seen between serum prolactin and progesterone levels (r=-0.6404, p<0.005). By the administration of bromocriptine, the luteal phase period of the pateints was prolonged significantly (p<0.005) and the mid-luteal serum estradiol and progesterone levels also showed significant increase (p<0.005, p<0.005).
    From these facts, it was concluded that the luteal function of these patients were disturbed even by the transient increase of serum prolactin levels and suggested that the transient increase of serum prolactin levels might suppress the luteal function directly. And the administration of bromocriptine was very effective to improve the luteal insufficiency of these patients.
  • 合成ホ乳類LH-RHとトリLH-RHとの比較
    高橋 優四郎, 宮本 薫, 長谷川 喜久, 五十嵐 正雄
    1986 年 62 巻 2 号 p. 126-139
    発行日: 1986/02/20
    公開日: 2012/09/24
    ジャーナル フリー
    Recently, Miyamoto et al and King et al, independently isolated chicken LH-RH and determined its chemical structure as [Gin8] LH-RH. In this report, the in vivo effect of synthetic chicken LH-RH on the release of LH and FSH and ovulation in rats was investigated.
    A single i.v. injection of chicken LH-RH, as well as mammalian LH-RH, induced a significant increase of plasma LH levels at 15 min after injection in adult male rats. Plasma LH levels then declined at 30 min to 60 min and returned to basal levels at 120 min.
    The biological potency of chicken LH-RH estimated from plasma LH levels at 15 min after injection in adult male rats by parallel line assay was 4.1% of that of mammalian LH-RH.
    It was likely that the activity of chicken LH was shorter in duration on the LH secretion as compared with that of mammalian LH-RH because of quickly decreased plasma LH levels.
    Plasma FSH levels were also increased, but the increment of FSH was not so obvious as compared with that of LH. Plasma FSH levels reached a plateau at 15 min and did not return to basal levels at 120 min in either the chicken LH-RH injection groups or the mammalian LH-RH injection groups.
    The chicken LH-RH was able to induce an increase of plasma LH and FSH and ovulation in pentobarbital-blocked, proestrous female rats. The biological potency of chicken LH-RH estimated from plasma LH levels at 15 min after injection in pentobarbital-blocked, proestrous female rats was 2.2% that of mammalian LH-RH. The ovulation-inducing potency of chicken LH-RH estimated from ED50 was about 2.1% of that of mammalian LH-RH.
    It is noteworthy that chicken LH-RH has a LH and FSH releasing and ovulation inducing-activity on rats in vivo, but its biological potency is weaker and of shorter duration compared with that of mammalian LH-RH, although the chemical structure of chicken LH-RH is different from that of mammalian LH-RH.
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