Parasympathetic nerve activity and hypoxic-ischemic brain damage in the developing fetus
Project/Area Number |
24592476
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Research Category |
Grant-in-Aid for Scientific Research (C)
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Allocation Type | Multi-year Fund |
Section | 一般 |
Research Field |
Obstetrics and gynecology
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Research Institution | University of Miyazaki |
Principal Investigator |
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Project Period (FY) |
2012-04-01 – 2015-03-31
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Project Status |
Completed (Fiscal Year 2014)
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Budget Amount *help |
¥5,070,000 (Direct Cost: ¥3,900,000、Indirect Cost: ¥1,170,000)
Fiscal Year 2014: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2013: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2012: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
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Keywords | 低酸素虚血性脳障害 / 副交感神経 / アセチルコリン受容体 / マイクログリア / 炎症性サイトカイン / 胎児心拍数細変動 / アセチルコリン受容体刺激 / 心拍数細変動 / 低酸素性虚血性脳障害 / 脳保護作用 / 胎児心拍数モニタリング |
Outline of Final Research Achievements |
The fetus is parasympathetic nerve dominant in a relatively lower pO2 condition, which presumably serves as hypoxia-tolerance. To test this hypothesis, we used hypoxic-ischemic brain damage models of 7-day-old Wistar rats. As a result, acetylcholine receptor agonists improved brain damage, while its antagonists worsened them. In addition, microglia activation and inflammatory cytokine production are playing roles. Next, we used same animal models and recorded heart rate variability during repetitive hypoxic stresses, which is represented as parasympathetic nerve activity. Repetitive hypoxia resulted in decreased baseline and responsive variability in some animals, which is more often associated with later brain damage. These findings suggest that parasympathetic activation serves as hypoxia-tolerance and that its suppression can be detected by decreases in fetal heart rate variability during hypoxic insults.
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Report
(4 results)
Research Products
(20 results)
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[Presentation] 胎児心拍数モニタリング2014
Author(s)
鮫島浩
Organizer
中国四国参加婦人科学会学術集会
Place of Presentation
山口
Year and Date
2014-09-13 – 2014-09-14
Related Report
Invited
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