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55 巻, 6 号
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心身症における絶食療法時の反応と神経性食欲不振症について鈴木 三章, 上條 桂一1979 年 55 巻 6 号 p. 739-760
発行日: 1979/06/20
公開日: 2012/09/24
ジャーナル フリーThe hypothalamic-pituitary-adrenal axis was investigated in 33 patients with various psychosomatic diseases treated with fasting therapy for 11 days, and a comparative study was made between this group and 13 young women with anorexia nervosa.
The results obtained were as follows :
1) The administration of dexamethasone failed to suppress cortisol levels to a normal range in 14 out of 33 patients during fasting
2) The normal circadian rhythm of plasma cortisol was abolished in 9 out of 21 patients during fasting. Plasma cortisol concentrations were significantly elevated at any given time of the day, especially in the dexamethasone nonsuppressive patients.
3) The excretion of urinary 17-OHCS and 17-KS in the 24-hr samples after the oral administration of metopirone was significantly higher in fasting patients as compared with non-fasting patients. The response of plasma ACTH to metopirone showed a non-significant increase.
4) The circadian rhythm of ACTH responsiveness to metopirone administration was normal in patients during fasting.
5) The plasma cortisol response to β1-24 ACTH 0.25 mg im was significantly higher in fasting patients as compared with non-fasting patients.
6) The basal urinary 17-OHCS and 17-KS in the 24-hr sample displayed a biphasic fluctuation with the peaks at 3 and 6 days after the initiation of fasting,
7) The cortisol metabolic clearance rate in fasting patients was prolonged as compared with that in non-fasting patients.
8) After refeeding, pituitary adrenal functions returned to normal in all patients.
9) Anorexia nervosa patients, non-suppressive to dexamethasone, demonstrated elevated plasma cortisol levels, normal responses to metopirone and ACTH, with a decreased excretion of urinary 17-OHCS and 17-KS.
It is concluded that high levels of plasma cortisol in both fasting and anorexia nervosa were caused by abnormalities of the negative feedback mechanism and prolongation of cortisol metabolic clearance rate. In addition, it was noted that patients exposed to fasting revealed an adrenocortical hyperfunction.抄録全体を表示PDF形式でダウンロード (1725K) -
高山 精次1979 年 55 巻 6 号 p. 761-775
発行日: 1979/06/20
公開日: 2012/09/24
ジャーナル フリーThe ovulation mechanism was studied on the basis of those biochemical events occurring in the ovarian follicle wall which lead to the bursting of the top of the follicle.
Bovine follicles were divided into the following 5 groups according to their sizes : 5 (4-6) mm in diameter, 10 (8-12) mm, 15 (13-17) mm, 20 (18-22) mm and 25 (over 25) mm. Protease activity in the follicle wall was estimated by measuring trypsin activity of hydrolyzing casein. Plasmin activity was determined by the fibrin plate method. The experiments revealed that the larger the follicle was in size, the higher protease activity it showed. Mature follicles with diameters of 15-25 mm were found to have the highest protease activity in their walls. However, the activity of very large follicles whose diameters were over 25 mm was quite low. Protease activity at the follicular top was remarkably high as compared with that of the surrounding area. As the follicles grew larger, their walls became thinner, especially at the top. While follicle-stimulating hormone (FSH), pregnant mare serum (PMS), human chorionic gonadotropin (HCG), and progesterone had a tendency to enhance protease activity to a small degree, estrone specifically inhibited the activity almost completely.
When HCG was administered to mature rabbits weighing 3-3.5 kg, ovulation occurred within 10 hrs after the administration. Meanwhile, when transamine (trans-4-aminocyclohexane carboxyamide), an antiplasmin, was administered concomitantly with HCG, ovulation was completely inhibited in spite of mature follicles being present in the ovaries. Serial administration of transamine after HCG resulted in complete inhibition of ovulation for 7 hrs after the administration. However, 1.5 (the average number) of more than 10 mature follicles ovulated 8 hrs after. One hour later, the number of ovulating follicles was increased to 5. These findings indicate that protease begins to show its ovulation-promoting action only 8 hrs after HCG administration; that is, the latent period of 7 hrs is necessary for protease production.
Transamine is supposed not to have any effect on plasmin already produced, but to act specifically on the proactivator or activator necessary for the production of plasmin. On the other hand, HCG was unlikely to directly affect plasmin formation, for, the addition of HCG to the fibrin plate only slightly helped activate plasmin.
In view of an activator and/or inhibitor involved in the control mechanism for protease activity, quantitative changes of a plasmin inhibitor were studied as the ovarian follicles grew larger. The amount of the inhibitor normally decreased with the growth of the follicles, but it markedly increased in follicles with ovulation disturbances.
It may be rational to suppose that the follicle wall is digested by protease with the result of disruption of ovulation, and that ovulation disturbance results not only from deficiency of LH secretion or imbalance between FSH and LH secretions, but also from de-creased protease activity or deficiency of the enzyme in the ovarian follicle wall.抄録全体を表示PDF形式でダウンロード (1273K) -
森 昌朋, 大島 喜八, 丸田 栄, 福田 均, 下村 洋之助, 小林 功, 小林 節雄, 若林 克己1979 年 55 巻 6 号 p. 776-786
発行日: 1979/06/20
公開日: 2012/09/24
ジャーナル フリーTo examine the physiological significance of TRH on the pituitary-thyroid axis, hypothalamic TRH contents and degradating activities in in vitro systems were measured in rats with various thyroid statuses. Furthermore, the influences of active and passive immunization with TRH were studied in normal and thyroid deficient rats.
The hypothalamic TRH content was not significantly altered by thyroidectomy and T4 administration. The rate of TRH degradating activity determined in vitro was increased by the serum of T4-treated rats, while it was decreased by the serum of thyroidectomized rats, as compared with normal serum. On the other hand, the administration of anti-TRH rabbit serum significantly suppressed the elevation of serum TSH following thyroidectomy, although the decreased TSH level in passively immunized rats was still higher than in normal rats. No suppression of serum TSH levels was observed by the administration of normal rabbit serum (NRS) and anti-LH-RH serum. Moreover, the serum TSH rise following PTU treatment was blunted by active immunization with TRH. In addition, serum TSH levels of anti-TRH serum-injected rats was further decreased by T3 administration, and the rate of decline in serum TSH levels was facter than that of NRS-injected rats.
The results of the present study suggest the physiological significance of endogenous TRH in the regulation of TSH secretion. In addition, TRH degradating activity may be influenced by various degrees of thyroid function ana thereby regulate the acting time of TRH on the pituitary level as the site of TSH secretion. Thus, it has been proposed that TRH may affect a “set-point” of the pituitary to induce TSH secretion in response to circulating thyroid hormone concentrations.抄録全体を表示PDF形式でダウンロード (863K) -
浜田 昇, 伊藤 國彦, 三村 孝, 森 秀樹, 百渓 尚子, 西川 義彦1979 年 55 巻 6 号 p. 787-796
発行日: 1979/06/20
公開日: 2012/09/24
ジャーナル フリーIn order to investigate the role of aldosterone in the pathogenesis of hypokalemic periodic paralysis, changes in serum cortisol (SC), aldosterone (SA) and plasma renin activity (PRA) were observed during 4 spontaneous attacks of paralysis in 3 thyrotoxic patients.
The patient, H.I., a 26-year-old man, was admitted to Ito Hospital in April, 1977, for paralysis of the extremities. He had a subtotal thyroidectomy for Grave's disease in June, 1974. Physical examination revealed that he had a clear consciousness and no speech disturbance, but he was unable to lift his extremities against gravity.
Laboratory findings on admission showed that serum thyroxine (T4) was 25.0-μg/ dl, triiodothyronine (T3) 720 ng/dl, K 2.4 mEq/L, SC 8.1 μg/dl, SA 2.0 ng/dl and PRA 5.3 ng/ml/hr. Immediately after recovery from the paralysis by the oral administration of aspara K 20 mEq, serum K was 3.4 mEq/L, SC 8.1 μg/dl, SA 2.0 ng/dl and PRA 3.9 ng/ml/hr. The next morning, serum K was 4.5 mEq/L, SC 8.7 mg/di, SA 5.0 ng/dl and PRA 1.0 ng/ml/hr. A similar attack of paralysis was observed after 6 months with serum K 2.0 mEq/L and SA 5.0 ng/dl.
The patient, M.O., a 32-year-old man, was admitted to Ito Hospital in January, 1978, by ambulance for paralysis of the legs. Physical examination revealed a well-nourished man with a diffuse goiter. He had normal strength in the upper extremities but was unable to lift the lower extremities against gravity.
Laboratory findings on admission showed that serum K was 1.8 mEq/L, SA 6.0 ng/dl, PRA 3.3 ng/ml/hr, T365 ng/dl and T4 25.0-μg/dl. Immediately after recovery from the paralysis by drip infusion of aspara K 6 mEq dissolved in 150 ml of 10% maltose, serum K was 3.7 mEq/L, SA 7.0 ng/dl and PRA 6.1 ng/dl. The next morning, serum K was 4.0 mEq/L, SA 6.0 ng/dl and PRA 3.6 ng/ml/hr.
The patient, C.W., a 35-year-old man, was admitted to Ito Hospital in January, 1977, for palpitation and weight loss. Physical examination revealed that he was a man of average build with a diffuse goiter, and that he had normal muscle strength in the extremities. A thyroid function test showed a T3 of 745 ng/dl, T4 of 25.-μg/dl and 131 I-thyroidal uptake (24 hr) of 65%.
On the 7th day after admission, he complained of an inability to stand up from a squatting position. At this time, serum K was 3.6 mEq/L, SC 12.8 μg/di, SA 8.0 ng/dl and PRA 2.3 ng/ml/hr. Without treatment, complete flaccid paralysis was observed at 2 hours after dinner with serum K 2.3 mEq/L and SA 1.0 ng/dl. After a spontaneous recovery from the paralysis, serum K was 4.1 mEq/L, SA 7.0 ng/dl and PRA 0.7 ng/ml/hr.
Serum cortisol, aldosterone and plasma renin activity were measured by radioimmunoassay using commercial kits (Cortisol RIA kit, Eiken, Renin RIA kit, Dainabot, aldosterone 3H kit, Midori Juji, Japan).
These findings suggested that aldosterone may not play a role in the pathogenesis of thyrotoxic periodic paralysis and may also not be an aggravating factor in paralysis induced by an unknown cause.抄録全体を表示PDF形式でダウンロード (886K) -
今北 哲雄, 熊坂 高弘, 鈴木 明, 斎藤 幹1979 年 55 巻 6 号 p. 797-804
発行日: 1979/06/20
公開日: 2012/09/24
ジャーナル フリーWe extracted the immunoreactive luteinizing hormone-releasing hormone (IR-LHRH) from villous and plasma in the first trimester of pregnancy with 0.2N acetic acid and the florisil absorbtion method. Recovery rate was 40.0 ± 4.08% in the former and 62.5 ± 9.5% in the latter, respectively. These IR-LHRH were measured by radioimmunoassay, which showed sensitivity from 5 to 500 pg/ml. The villous IR-LHRH was compared with synthetic LH-RH by a dilution curve in different concentrations and the column gel filtration of sephadex-G25. The dilution curve of synthetic LH-RH and sample material showed a significant correlation, and the elution time of villous IR-LHRH on the column was something faster than that of synthetic LH-RH. The concentration of villous IR-LHRH showed 20-100 pg/0.1g dry weight in the first trimester of pregnancy, and the peak was at 9 weeks of normal pregnancy and at 8 weeks of inevitable abortion respectively, but these IR-LHRH levels were not changed between pre- and post-dilation and curettage. From this evidence, we considered that IR-LHRH show activity of the local hormone in villous tissue similar to somatostatin.抄録全体を表示PDF形式でダウンロード (610K) -
肝Testosterone 5α-, 5β-Reductaseに及ぼす各種薬物の効果とその調節因子について田中 節子, 本間 誠次郎, 神戸川 明1979 年 55 巻 6 号 p. 805-816
発行日: 1979/06/20
公開日: 2012/09/24
ジャーナル フリーThe administration of chlormadinone acetate or estradiol benzoate to male rats causes a significant fall in plasma testosterone levels and an increase in the activity of hepatic testosterone A ring reduction. The metabolism of testosterone-4--14C was studied in the microsomal fraction, and 105,000 × g supernatant fraction of the livers of normal male and hypophysectomized male rats that had been treated with chlormadinone acetate, estradiol benzoate, phenobarbital, or 3-methylcholanthrene.
100 mg/kg of chlormadinone acetate or 1 mg/kg of estradiol benzoate was administrated to separate groups of male rats daily for 5 weeks and 9 days, respectively. The conversion of testosterone to 5α-dihydrotestosterone in the hepatic microsome was increased approximately 2-3 times by the treatment of chlormadinone acetate or estradiol benzoate. However, the 5β-reductase in 105,000 × g supernatant was little influenced by chlormadinone acetate and estradiol benzoate. When estradiol benzoate was administered to hypophysectomized male rats, 5α-reductase activity was not induced. These findings indicate an essential role of the pituitary gland in the regulation of _??_4-5α-reductase. On the other hand, when phenobarbital or 3-methylcholanthrene, inducer of the drug oxidizing enzymes in the liver, was administered to normal and hypophysectomized rats, there was a substantial depression of 5α-reductase activity without any effects on 5β-reductase. However, the microsome caused a 50% increase in aniline hydroxylation activity. The results showed that phenobarbital not only enhanced the oxidative drug metabolism in the liver as expected but also decreased hepatic _??_4-5α-reductase activity to increase the ratio of 5β/5α-metabolites formed from testosterone-414C. Further, to test whether or not chlormadinone acetate induces the formation of the 5α-reduced derivative of progesterone in the hepatic microsome, we studied the conversion of progesterone-4-14C to 5α-dihydroprogesterone in vitro. The hepatic microsome, which was bubbled through CO gas for 2 min, gave 5α-dihydro-progesterone as the major metabolite of progesterone-4-14C. And the conversion of progesterone to 5α-dihydroprogesterone was also enhanced approximately 3 times by the treatment of chlormadinone acetate (100 mg/kg) for 5 weeks.
The hepatic 5α-reductase induced by chlormadinone acetate was able to hydrogenate not only testosterone, but also C21-_??_4-3-oxosteroid such as progesterone. Based on these results, we discussed a regulation system of hepatic testosterone-5α-reduction.抄録全体を表示PDF形式でダウンロード (1940K) -
下山 貞雄1979 年 55 巻 6 号 p. 817-830
発行日: 1979/06/20
公開日: 2012/09/24
ジャーナル フリーAdult male wistar rats averaging 200 g each were subjected to food removal for 1-6 days or fed ad libitum throughout (controls). Plasma GH levels and pituitary GH contents were measured by radioimmunoassay. The GH responses to intravenous injection of TRH (2.5 μg/100 g B.W.), PGE1 (5μg/100 g B.W.), LH-RH (1 μg/100 g B.W.) and Chlorpromazine (CPZ, 100 μg/100 g B.W.) were tested under urethane anesthesia.
Circulating GH levels were significantly increased by prolonged starvation, while pituitary GH contents progressively decreased with increased periods of starvation. In addition, following the TRH administration, plasma GH levels increased in starved rats compared to the control rats. A similar effect was also observed with PGE1. In contrast, the administration of CPZ, which was reported to act at the hypothalamic level, failed to potentiate GH release in starved rats under urethane anesthesia.
These observations suggest an increased susceptibility of starved rats to urethane anesthesia with the administration of TRH and PGE1 in the GH secretory mechanism. In addition, the fact that no further potentiation of GH release was observed by CPZ treatment may indicate an abnormality of the hypothalamic dopaminergic mechanism in starved animals.抄録全体を表示PDF形式でダウンロード (1302K)
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