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https://hdl.handle.net/20.500.14094/0100488743
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2026-08-11
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説明
32-6_179-195 (fulltext)
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3.09 MB
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ファイル出力
メタデータID
0100488743
アクセス権
open access
出版タイプ
Version of Record
タイトル
CNS CHANGES IN THE MECONIUM ASPIRATION SYNDROME
著者
著者名
MIYATA, HIROYOSHI
著者名
HIROSHI, ITOH
言語
English (英語)
収録物名
The Kobe journal of the medical sciences
巻(号)
32(6)
ページ
179-195
刊行日
1986-12
抄録
Pathological study on the central nervous system (CNS) were performed in cases of the meconium aspiration syndrome (MAS) in order to elucidate hypoxic changes of the neonatal CNS. Thirty-eight autopsied MAS cases showed clinically severe and prolonged hypoxia during the perinatal period, and pathologically severe MAS changes in more than 2 lobes. The brain/body weight ratios at autopsy were estimated in short-lived cases within 7 days, and they were classified into group A showing higher ratios than normal control ratios, and group B showing lower than normal ratios in order to evaluate the effects of brain edema. There were degeneration and decrease of neuronal cells, and the edematous or spongy changes of the stroma in addition to various degrees of degeneration in axons and myelinated fibers in the brains of all cases. Those changes were more severe and more widely spread in group A especially in the cerebral gray matter and the cerebellum. Thus it is considered that brain edema injures the hypoxic brain and that the cerebral gray matter and the cerebellum are not easily to be injured by hypoxia but to be injured by edema. The brains in long-lived cases of over 14 days showed mostly diffuse and marked edema with neuronal necrosis and GFAP positive microglial infiltration in the gray and white matters, and simultaneously revealed more marked atrophy of the whole brain than that of both short-lived groups. So it is proved that the long lasting hypoxia affects the whole brain severely.
キーワード
meconium aspiration syndrome (MAS)
hypoxic brain
perinatal brain damage
neuropathological study
カテゴリ
The Kobe journal of the medical sciences
>
32巻
>
32巻6号(1986-12)
紀要論文
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資源タイプ
departmental bulletin paper
ISSN
0023-2513
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NCID
AA00711740
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