| Project/Area Number |
24591613
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Embryonic/Neonatal medicine
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| Research Institution | Tokyo Women's Medical University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
KITAHARA Syuji 東京女子医科大学, 医学部, 助教 (40510235)
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| Project Period (FY) |
2012-04-01 – 2016-03-31
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| Project Status |
Completed (Fiscal Year 2015)
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| Budget Amount *help |
¥5,070,000 (Direct Cost: ¥3,900,000、Indirect Cost: ¥1,170,000)
Fiscal Year 2014: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2013: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
Fiscal Year 2012: ¥2,730,000 (Direct Cost: ¥2,100,000、Indirect Cost: ¥630,000)
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| Keywords | 慢性肺疾患 / 早産児 / 肺胞微小血管 / 血液空気関門 / 血管内皮細胞 / 微小血管障害 / 肺高血圧 / Angiopoietin-1 / 肺胞微小循環 / 血管再生 |
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| Outline of Final Research Achievements |
To elucidate the morphological characterization of the mechanisms for pulmonary vascular disease secondary to bronchopulmonary dysplasia (BPD), we studied the ultrastructural changes of the pulmonary microvasculature (PV) by using newborn mice lungs exposed to 14 days’ hyperoxia and subsequent seven days of normal air replacement conditions. The ultrastructure of PV in the hyperoxia-exposed lung had the characteristics of collapsed capillary lumen due to abnormal morphology of endothelial cells (ECs) with heterogeneously thick cytoplasm, and thick blood-air barriers (BABs), compared to air-control. Moreover, those abnormal ultrastructural changes of ECs persisted even after seven days of room air replacement conditions. These results indicate that the circulatory collapse at the alveolar capillary level might cause high vascular resistance, and that thick BABs might worsen hypoxemia and hypercapnia, the both of which finally can be the cause of secondary pulmonary hypertension in BPD.
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