マウスの胎生期副腎皮質に関する実験的研究
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概要
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The design of this work is firstly to clarify the functional development of the fetal adrenal, secondly to detect endocrine interrelationships of the adrenal between the fetus and the mother, and thirdly to know whether or not the X zone of mouse adrenal is a remnant of the so-called "fetal cortex", on the basis of the histologic and experimental studies. (1) Functional development of the fetal adrenal cortex. The sudanophilic granules first appeared in cortical cells on the 16 day stage. Hypertrophy of mitochondria and the first appearance of ascorbic acid in the cells occurred coincidently on the 19 day stage. These findings seem to support the view of a rapid increase of the functional activity of the fetal adrenal between the 18 day and the 19 day stages. After maternal adrenalectomy, almost no change was caused in the fetal adrenal until the 18 day stage, whereas on the 19 day stage the ratio of the fetal adrenal volume to the body weight significantly augmented with a decrease of sudanophilic lipid content in the cells of the intermediate zone. The adrenals of fetuses decapitated in utero became smaller than those of litter-mate controls: the cortex narrowed, the lipid droplets in cells being larger and more widely separated from one another. These changes in volume and histology of the adrenal were accentuated as the period of absence of the hypophysis lengthened, and especially they stood out in those cases in which the period of absence of head included the interval from the 18 day to the 19 day stages. The result of experiment of fetal decapitation suggests that the adrenalstimulating activity of the fetal hypophysis increases rapidly up to the 19 day stage. These various findings may lead to the conclusion that the critical period of the onset of secretory activity lies probably between the 18 day and the 19 day stages of the embryonic life. However, in regard to the role of the adrenal in the glycogen storage of the fetal liver, histologic studies revealed that the glycogen content of the liver cells showed no change under a hypo function of the fetal adrenal following fetal decapitation. Maternal adrenalectomy and hypophysectomy resulted in no change of the glycogen content of the fetal liver cells. (2) Endocrine interrelationships of the adrenal between the fetus and the mother. Maternal hypophysectomy caused almost no change in volume and histology of the fetal adrenal. The large amount of ACTH reached the fetus through the placental barrier and eventually caused a fetal adrenal hypertophy. Small doses of ACTH did not show any stimulation of the fetal adrenal. Formalin, when injected to the mother, enlarged the maternal adrenal and reduced the volume of the fetal adrenal. The interpretation that an increased amount of maternal corticoids depresses the activity of the fetal pituiatry-adrenal axis and that the fetal adrenal enlargement following maternal adrenalectomy is caused by the elevation of the titer of adrenocorticotropin from the fetal pituitary could be applied also to the case of the mouse. The fetal adrenals grew progressively up to the final day of pregnancy and the volume of the adrenal was reduced at birth. This reduction in volume appeared to be due to the shrinkage of the cortical cells of the adrenal. The adrenal of the fetal mouse decreased in volume after maternal ovariectomy. Progesterone, which was administered for the purpose of preventing abortion following ovariectomy, exerted little effect on the fetal adrenal. Control animals of this experiment were subjected to sham operation. Likely, the atrophy of the fetal adrenal in utero occurs in the absence of some ovarian substances. Probably, the neonatal involution of the adrenal results from the loss of or the change in several maternal hormones, including ovarian hormones, or from the interrelationships among them. (3) Histologic development of the fetal mouse adrenal. The anlage of the adrenal of the mouse appeared first on the 12 day stage of the embryonic life as thickening of the coelomic epithelium on the craniomedial side of the genital ridge. The cells of the anlage from the 13 day stage onward had rich and eosinophilic cytoplasms and arranged in irregular cords. The capsule appeared blastemal and showed possibly a new addition of cortical cells. On the later stages of the prenatal life, the blastemal capsule on the coelomic side turned to the fibrous connective tissue and seemed to cease apposing new cortical cells. The eosinophilic cortical gland mass was invaded and separated irregularly by the medullary elements about 15 day stage, which caused thereafter a branched appearance of the inner part of the cortex. Except the peripheral part, the cortical tissue consisted entirely of large eosinophilic cells which appeared all alike both in morphology and in stainability: the cortex did not show a striking esinophilia of the innermost part alone, showing no sign of down-oppression of the early differentiated cortical tissue. When the medullary elements were mostly centralized, the cortex was disposed vaguely in three zones, i.e., the outer (corresponding to the postnatal glomerulosa), the intermediate (corresponding to the postnatal fasciculata) and the innermost branched zone (corresponding to the postnatal inner fasciculata). The cells of the innermost branched zone were identical both in morphology and in stainability with those of the intermediate zone and composed no special different zone. Thus, the early postnatal adrenal tissue kept merely a continuation of the fetal situation, only the medullary tissues became more definitely centralized. It does not seem to be guaranted that only the X zone, which appears on the later period of the infantile stage, is a remnant of the early adrenal cortex. Probably, the X zone is formed as a result of morphologic or functional changes of the innermost part of the postnatal adrenal cortex.
- 大阪府立大学の論文
- 1963-03-31