| 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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| 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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