2004 Fiscal Year Final Research Report Summary
Studies on the protective mechanism of the fetal brain against hypoxic-ischemic insult during delivery
| Project/Area Number |
15390507
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Obstetrics and gynecology
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| Research Institution | Yamaguchi University |
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Principal Investigator |
NAKAMURA Shoji Yamaguchi Univ., School of Med., Professor, 医学部, 教授 (80112051)
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| Co-Investigator(Kenkyū-buntansha) |
SAKATA Yoshiyuki Yamaguchi Univ., School of Med., Assistant Professor, 医学部, 講師 (10034927)
FUJIOKA Takashi Yamaguchi Univ., School of Med., Assistant Professor, 医学部, 講師 (50304473)
ISHIKAWA Akinori Yamaguchi Univ., School of Med., Research Associate, 医学部, 助手 (40363098)
TSUCHIMOCHI Hirotsugu Yamaguchi Univ., School of Med., Research Associate, 医学部, 助手 (60379948)
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| Project Period (FY) |
2003 – 2004
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| Keywords | asphyxia / fetal brain / umbilical cord occlusion / NO / superoxide dismutase / delivery / ischemia / oxygen |
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| Research Abstract |
Although the fetuses experiences severe hypoxia and ischemia during delivery, the fetal brain is protected from hypoxic-ischemic insults by unknown mechanism. In a previous study, we found that at-term rat fetuses revealed a paradoxical rise in brainstem PO2 following umbilical cord occlusion, while brainstem blood flow was markedly reduced. The present experiments were designed to investigate the mechanism of this paradoxical rise in brainstem PO2 of at-term fetuses. There are two possible explanations for this phenomenon : The paradoxical rise in brainstem PO2 is due to 1) de novo generation of O2 in the brainstem or 2)O2 release from a reservoir other than blood.
To investigate possibility 1), we performed several experiments, including a) the effects of a superoxide dismutase (SOD) inhibitor on the paradoxical rise in brainstem PO2, b) Quantitative analysis of fetal brain SOD by immunoblot and c) Real-time measurement of nitrogen monoxide (NO) in the fetal brainstem following umbilical cord occlusion. In these experiments, the possibility was examined that O2 is produced from oxygen radicals which generate during hypoxic-ischemic insults. However, we did not find any evidence supporting this possibility. To investigate possibility 2), we searched chemical substances which can bind to O2. It was found that there was no such a substance in the adult rat brain, but the fetal brain remains to be investigated in future experiments. Although we also performed a morphological study on blood vessels in the fetal brain in relation to hypoxia, no significant change was found between control and hypoxia groups.
In summary, we could not reach a conclusion on the paradoxical rise in brainstem PO2 of at-term fetuses, although a variety of experiments were performed.
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