巻号一覧
前身誌
39 巻, 11 号
選択された号の論文の5件中1～5を表示しています
- |<
- <
- 1
- >
- >|
-
天津 實1964 年 39 巻 11 号 p. 1009-1012,1003
発行日: 1964/02/20
公開日: 2012/09/24
ジャーナル フリーIn the previous paper, aromatization of dehydroepiandrosterone, 4-androstenedione and testosterone was reported. In this paper, two 17α-methyl-steroids were studied about the possibility of their aromatization in vitro.
Methods were similar to those described in the previous paper, but 17α-methyl-19-nortestosterone and 17α-methyl-testosterone were used as substrate. Phenolic extract obtained in 8 experiments with 17α-methyl-19-nortestosterone was pooled and chromatographed on paper in the benzene-ligroin-methanol-water system for 4 hours at 25°C.
Areas corresponded in its mobility with authentic 17α-methyl-estradiol were eluted by methanol and rechromatographed several times in the same system.
The compound thus obtained was compaired with authentic 17α-methyl-estradiol in its UV-absorption spectrum, sulfuric acid chromogen spectrum, alcohol-sulfuric acid (1 : 2) chromogen spectrum, and 2% hydroquinone-65% sulfuric acid chromogen spectrum. All these findings revealed, the compound obtained in the incubation of 17α-methyl-19-nortestosterone with human placental homogenate was 17α-methyl-estradiol.
Experiments with 17α-methyl-testosterone also resulted the formation of 17α-methyl-estradiol in the same criteria.抄録全体を表示PDF形式でダウンロード (478K) -
長井 勇1964 年 39 巻 11 号 p. 1013-1030,1004
発行日: 1964/02/20
公開日: 2012/09/24
ジャーナル フリーEither a 'foreward' or 'backward failure' theory has not cleary explained the pathogenesis of edema in congestive heart failure. Attention has been directed towards Aldosterone as a results of many reports that the excretion of this steroid in urine is increased in a number of diseases which are accomanied by the formation of edema as well as congestive heart failure.
In the present study urinary Aldosterone was determined in patients with congestive heart failure, except for hypertensive subjects, by a modified procedure of Mattox.
Relation between urinary Aldosterone and many kinds of clinical findings were investigated. In addition, successive determinations of urinary Aldosterone were made to determine how to relate this steroid to the changes of electrolyte excretion, circulatory dynamics, and other clinical findings induced by treatments.
The results obtained were as follows :
1) Urinary Aldosterone was increased as the grade of failure advanced.
2) A higher excretion of Aldosterone in urine of patients with right ventricular failure was observed than in those of left ventricular failure.
3) There were no differences in the levels of Aldosterone excretion between patients with peripheral edema and those without.
4) It was observed that there is a relation between the amounts of Aldosterone in urine and circulation time, filtrtion fraction, intra-red cellular sodium concentration and intra-red cellular Na/K ratio respectively. Inverse relation was noted among the levels of Aldosterone in urine and intra-red cellular potassium concentration, urinary Na/K ratio and urinary 17-OHCS. Observations on urinary sodium and potassium excretion, serum sodium and potassium concentration, serum Na/K ratio, and venous pressure in relation to the amounts of Aldosterone excreted in urine indicated that there is little relationship between them respectively.
5) When Desoxycorticosterone acetate was administered to normal subjects and patients with congestive heart failure there were no diffeences in the mode of response to DOCA injection between the two groups except for weight gain which was much pronounced in patients with congestive heart failure.
6) Successive determinations of urinary Aldosterone throughout the course of treatment disclosed that :
i) coincident with diuresis or saluresis the amount of Aldosterone in urine was markedly increased.
ii) in cases where the gross edema completely subsided, the levels of Aldosterone in urine were gradually decreased and venous pressure and circulation time returned to normal. In cases, however, where a favourable effect was observed on urine flow a nd electrolyte excretion but where a little edema was left on lower extremities, no decrease of urinary Aldosterone was noted and venous pressure and circulation time improved a little as compared with those in pre-treatment period.
7) The effect of SC-9420 (doses about 1000 mg/day) on urine flow and electrolyte excretion in congestive heart failure was favourable, and combined administration with Hydroflumethiazide achieved marked diuresis.抄録全体を表示PDF形式でダウンロード (1945K) -
黒島 晨汎1964 年 39 巻 11 号 p. 1031-1039,1006
発行日: 1964/02/20
公開日: 2012/09/24
ジャーナル フリーThe effect of vasopressin on the thyroid activity was studied in rats, measuring T/S ratio, thyroidal 131I uptake and serum PB131I.
Neither single doses of Pitressin, 60 mU. per 100 gm. body weight, nor successive administrations of Pitressin tannate, 100 and 400 mU. per 100 gm. body weight daily for 3 days, caused any significant change in the T/S ratio in rats kept at 20°C. Exposure of rats to a cold environment of 10°C for 1 week resulted in a marked increase in the T/S ratio as well as the thyroid gland weight. Chronic treatment with Pitressin in a dose of 40 mU. per 100 gm. body weight twice a day during the period of cold exposure brought about a suppression of the rise in T/S ratio due to cold exposure.
The serum PB131I level was maintained at approximately the same level during the period of repeated blood collections which was possibly due to minor surgical stress of blood collection. Pitressin in a dose of 100 mU. per 100 gm. body weight but not synthetic lysine vasopressin, caused a progressive decrease in the serum PB131I level. After hypophysectomy the serum PB131I level decreased progressively with time. Pitressin had no effect on this decrease of PB131lI in these rats. In hypophysectomized rats, the rise of PB131li followed by exogenous TSH, 50 mU. per 100 gm. body weight, was suppressed by the simultaneous administration of Pitressin, 100 mU. per 100 gm. body weight, but not by that of synthetic lysine vasopressin.
Administration of ACTH, methylthiouracil, epinephrine, Dibenzline, and Ismelin as well as adrenal medullectomy did not affect PB131I level under the conditions used.抄録全体を表示PDF形式でダウンロード (1184K) -
第1編 糖尿病の食餌負荷及びSulfonylurea剤投与による血中NEFAの変動胡桃 彰1964 年 39 巻 11 号 p. 1040-1051,1007
発行日: 1964/02/20
公開日: 2012/09/24
ジャーナル フリーI. Serum lipids of diadetics on 3 principal nutrients.
Diabetic fasting for 15 hours were given orally with butter, salad oil, protein or glucose, 400 Cal. equivalent respectively, and, the serum total lipids, total pospholipid total cholesterol, NEFA and glucose were measured to 6 hours (immediate effects), and to a month (delayed effects) in which butter, salad oil or protein of 200 Cal. equivalent were added to the basic diet for a month.
1, Immediate effects ; The serum NEFA was first decreased and then increased by diet. There was a time lag observed between the healthy and the diabetics particular-ly on butter, salad oil. A similar pattern was shown for the serum total phospholipids.
2, Delayed effects ; The total cholesterol was increased throughout the cases and the elevation of C/P ratio was decreased in order of butter, salad oil and protein diet. Fasting blood sugar was increased by protein and butter diet.
II. The relation of serum NEFA to blood sugar.
Diabetic patients, fasting for 15 hours were given with 50 gm. glucose orally or 1 gm. of tolbutamide intravenously and the serum NEFA and blood sugar were measured.
1, No correlation was observed between fasting blood sugar and fasting NEFA, but higher the fasting blood sugar, the more prolonged the time lapse to reach the minimum of NEFA.
2, Tolbutamide brought the blood sugar in 60 minutes and the NEFA in 30 minutes to the minimum value. The higher the fasting NEFA, the more was it decreased by tolbutamide.抄録全体を表示PDF形式でダウンロード (1362K) -
第II編 Growth Hormone並にAnabolic SteroidのNEFA net balanceに及ぼす影響について胡桃 彰1964 年 39 巻 11 号 p. 1052-1075,1008
発行日: 1964/02/20
公開日: 2012/09/24
ジャーナル フリー1. The effects of bovine growth hormone on NEFA net balance.
Fat, heart muscle, liver or kidney tissue of normal male or alloxan diabetic rabbit, or adipose tissue of normal or hypophysectomized rat were buffered with Krebs-Ringer bicarbonate (pH. 7.4) containing 2% human plasma or 0.2% sesame oil emulsion besides and incubated for 2 to 4 hours at 37°C to measure NEFA in the medium.
1, Growth hormone (GH) (3-25μg/ml.), like insulin, inhibited the release of NEFA from the tissue and antagonized epinephrine or ACTH which accelerated the release. Similar action was observed of GH by adding in vitro to the medium or by pretreating the animal by injection. However, a large dose of GH contrarily diminuted the action.
2, NEFA tended to be decreased when GH was added to the medium with the suspension of liver mitochondria.
3, Epinephrine accelerated NEFA release from the adipose tissue but reversed against the heart muscle.
II. The effects of synthetic anabolic steroid (2-hydroxy methylene-17α-methyl-dihydro testosterone : HMD) on the net balance of NEFA.
1, HMD inhibited the release of NEFA from adipose tissue either by adding in vitro or by pretreating the rat.
2, Notwithstanding the fact, HMD antagonized the action of bovine GH or insulin to inhibit the release of NEFA.
3, GH revealed an additional action to insulin on NEFA release.
4, GH inhibited the accelerated release of NEFA by ACTH or epinephrine but not HMD.
On NEFA release, the action of bovine GH (Li's method) was similar and additional in action to each other with insulin and inhibited the release of NEFA which was accelerated by epinephrine or ACTH. HMD, a derivative of testosterone, inhibited as insulin did, the release of NEFA from adipose tissue both in vivo and in vitro. However, it inhibited the action of insulin and antagonized GH to inhibit the release of NEFA.
To conclude, GI-J, insulin and HMD give an appearance of having a common effect on the release of NEFA but the mechanism of actions apparently differ to each other.抄録全体を表示PDF形式でダウンロード (2641K)
- |<
- <
- 1
- >
- >|