Folia Endocrinologica Japonica
Online ISSN : 2186-506X
Print ISSN : 0029-0661
ISSN-L : 0029-0661
Volume 34, Issue 10
Displaying 1-5 of 5 articles from this issue
  • [in Japanese]
    1959 Volume 34 Issue 10 Pages 936-960
    Published: January 20, 1959
    Released on J-STAGE: September 24, 2012
    JOURNAL FREE ACCESS
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  • [in Japanese]
    1959 Volume 34 Issue 10 Pages 961-977
    Published: January 20, 1959
    Released on J-STAGE: September 24, 2012
    JOURNAL FREE ACCESS
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  • Shiro IINO
    1959 Volume 34 Issue 10 Pages 978-998,933
    Published: January 20, 1959
    Released on J-STAGE: September 24, 2012
    JOURNAL FREE ACCESS
    In order to investigate whether the autonomic innervation of the thyroid gland modifies the functional activity of this organ or not, the author studied the influence of the electrical stimulation of the cervical sympathetic nerve on the content of PBI131 in thyroidal venous blood in the dogs into which tracer dosis of I131 had been injected intravenously 5 or 6 days before experiment.
    The following results were obtained :
    1. After the stimulation of the right cranial cervical sympathetic ganglion, the concentration of PBI131 in thyroidal venous blood increased in 5 of 6 cases 2.1 to 7.61 times of the pre-stimulation level and the PBI131 output increased in 4 of 6 cases 1.47 to 3.52 times of the pre-stimulation level. In spite of the stimulation of the unilateral sympathetic nerve, the increase was observed bilaterally and no difference in particular between both sides. No significant influence was seen about the thyroidal venous blood flow by the stimulation.
    2. Following the stimulation of the ansa subclavia of the right sympathetic nerve, the concentration of PBI131 increased in 4 of 10 cases 1.72 to 2.22 times of the pre-stimulation level and the PBI131 output increased 2.5 times of the pre-stimulation level in one of 6 cases. In the remaining 4 cases the exact output could not be calculated because of the reduced thyroidal venous blood flow. Such increases were observed bilaterally and no difference in particular between both sides. No significant influence was seen about the blood flow through the thyroid gland by the stimulation.
    3. In hypophysectomized dogs with transplanted pituitary on their back, the concentration of PBI131 increased in 2 of 4 cases 1.75 to 2.9 times of the pre-stimulation level and the PBI131 output increased in 3 of 4 cases 1.61 to 1.91 times of the pre-stimulation level, following the stimulation of the right cranial cervical sympathetic ganglion. Such increases were observed only in the stimulated side.
    4. The results from these experiments indicate that the mechanism of the hormonal secretion of the thyroid gland can be modified by the cervical sympathetic nerves, mainly by fibers passing through the cranial cervical ganglion and occasionally by those passing through the caudal cervical ganglion or the stellate in part. It seems likely that the unilateral cervical sympathetic nerve can modify the functional activity of the thyroid gland bilaterally and that such a nervous control is rather secretomotoric than vasomotoric.
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  • Ken-ichi ISHIGAKI
    1959 Volume 34 Issue 10 Pages 999-1024,934
    Published: January 20, 1959
    Released on J-STAGE: September 24, 2012
    JOURNAL FREE ACCESS
    Recently the close relationship of catecholamines to the pathogenesis of hypertension has been brought up to our attention, but very little has been established in regard to the metabolism of catecholamines in human hypertension.
    The author estimated the catecholamines in plasma and urine in 250 cases under various conditions with regard to the relationship between blood pressure and these substances.
    Weil-Malherbe and Bone's fluorimetric method was employed to estimate plasma catecholamines, while urinary catecholamines were determined by Euler and Floding's method.
    Following results were obtained :
    1) In 69 healthy subjects and 157 patients with essential hypertension, plasma and urinary levels of noradrenaline (NA) had statistically significant correlation to systolic blood pressure. But no correlation was found between adrenaline (A) and blood pressure.
    2) For the same blood pressure levels, plasma NA was higher in aged subjects (over 60 years old) than in adult subjects (below 60 years old).
    3) In 18 patients with renal failure, no correlation was found between plasma NA and blood pressure.
    4) In 12 healthy subjects and 17 patients with essential hypertension, a good correlation was shown between plasma levels and urinary outputs of NA, but in 11 patients complicated with renal failure the pertinent relationship was not observed.
    5) In 2 hypertensive patients both catecholamines and blood pressure were markedly elevated at their usual work.
    6) In regard to diurnal variation of catecholamines in plasma and urine, there was no difference between 3 hypertensive patients and 3 healthy subjects, while the day-to-day variation of catecholamines in hypertension was more labile than in healthy subjects.
    7) The subcutaneous injection of NA in a dose of 0.5mg caused a definite pressor reaction in 3 hypertensive patients, while no reaction in 3 normotensive subjects and the excretion of NA injected was seemingly retarded in the former.
    8) In 15 hypertensive patients plasma levels of NA were considerably decreased after the treatment with hypotensors, and the effects of each hypotensors on plasmacatecholamines suggested the characteristic mechanism of action of these drugs.
    These evidences may be suggested that noradrenaline is closely related to the pathogenesis of hypertension.
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  • Kahei NISHI
    1959 Volume 34 Issue 10 Pages 1025-1055,935
    Published: January 20, 1959
    Released on J-STAGE: September 24, 2012
    JOURNAL FREE ACCESS
    Relationship between the hypothalamus and the pituitary-thyroidal system was investigated with respect to TRF, extracted from the anterior hypothalamus and urine, and the following results were obtained.
    (1) Consecutive intramuscular and single intravenous injections of the hypothalamic or the urinary extract elevated the blood level of TSH and PBI. The active principle accelerated the release of I131 from the thyroid.
    (2) Resection of the pituitary stalk induced hypofunction of the pituitary-thyroid system. TRF, if given in such operated cases, not only inhibited the hypofunction but rather stimulated this system.
    (3) When TRF was given to cases in which thyroidal function was depressed by hypophysectomy, any thyrotrophic effect was observed. It was thus indicated that TRF exerts its effect on the thyroid only through the mediation of TSH, namely, TRF is an accelerator of TSH release.
    (4) When the anterior hypothalamus was stimulated, the release of I131 from the thyroid was remarkably accelaerated only in bilaterally adrenalectomized rats.
    (5) When lesion was given in the anterior hypothalamus, extending from the supraoptic nuclei to to the suprachiasmatic nuclei basally and rostrally, remarkable hypofunction of the thyroid was induced. Thus the above mentioned site is considered to be the regulatory center for the thyroid. In this case, goitrogenic action of MTU was inhibited, but the administration of TRF exerted evident metabolic and goitrogenic action, giving stimulation to the pituitary-thyroid system.
    (6) The administration of TRF in a minute and a small dose elevated only the T/S level, but in a medium and a large dose it exerted both goitrogenic and thyrotrophic action. Namely it is considered that there are not two factors-growth factor and metabolic factor-in TSH, but only one thyroid-controlling factor (TRF) is present.
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