1988 Fiscal Year Final Research Report Summary
A study on ultrastractural changes of newborn brain before intraventricular hemorrhages
| Project/Area Number |
61570812
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| Research Category |
Grant-in-Aid for General Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Research Field |
Obstetrics and gynecology
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| Research Institution | Nippon Medical School |
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Principal Investigator |
KOSHINO Tatsuo Nippon Medical School Department of Obstetrics and Gynecology assistant Professor, 医学部, 助教授 (80089747)
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| Co-Investigator(Kenkyū-buntansha) |
OHTSUKA Shigeru Nippon Medical School. Department of Obstetrics and Gyhecology assistant, 医学部, 助手 (70185312)
TSUNODA Yutaka Nippon Medical School. Department of Obstetrics and Gyhecology assistant, 医学部, 助手 (20180036)
OGAWA Takayoshi Nippon Medical School. Department of Obstetrics and Gyhecology lecture, 医学部, 講師 (20177132)
WAKAOMI Yoshiki Nippon Medical School. Department of Obstetrics and Gyhecology lecture, 医学部, 講師 (50158573)
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| Project Period (FY) |
1986 – 1988
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| Keywords | subependymal hemorrhage / rat / fetus / glycogen / hypoxia / capillary permeability |
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| Research Abstract |
To investigate the causes of the onset of newborn intraventricular hemorrhages, perplacental ischemic loads were applied ultrastructural changes in the subependymal layer of the rat fetuses at 17,19,21days of gestation. And rat fetal brain glycogen content was measured. On the other hand rabbit newborn exposed nitrogenbox hypoxia for 5,10 minutes,and subependymal layer was observed by light and electron microscope, used by protain tracer of horseradish peroxidase(HRP).
The results obtained were as follows 1) The subependymal layer of the rat fetus was not well developed and structural maturation was not well confirmed. 2) The placental ischemic loads caused dilation of the intracellular space, elongation of the cellular processes of the cytoplasm. 3) Glycogen content increased from the 17th day, reaching a peak on the 19th day. 4) 10 minutes hypoxia caused destroyed astrocytes around capillary of subependymal layer, and HRP was passed out through endoterium tight junction in rabbit newborn
Ischemic, hypoxic damage might be caused of ultrastructual change of subependymal layer, such as edema of cell space and increase of cappilary permiability, and glycogen might be used an energy source to maintain brain tissue function during hypoxia.
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