2006 Fiscal Year Final Research Report Summary
The contribution and modulation of vascular endothelial growth factor for brain edema formation
| Project/Area Number |
17591634
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Anesthesiology/Resuscitation studies
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| Research Institution | Yamaguchi University |
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Principal Investigator |
IIDA Yasuhiko Yamaguchi Univ., Hospital, Research Associate, 医学部附属病院, 助手 (90304485)
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| Co-Investigator(Kenkyū-buntansha) |
SAEKI Hiroshi Yamaguchi Univ., Hospital, Research Associate, 医学部附属病院, 助手 (80379958)
YAMASHITA Atsuo Yamaguchi Univ., Hospital, Research Associate, 医学部附属病院, 助手 (50379971)
ISHIDA Kazuyoshi Yamaguchi Univ., School of Medicine, Research Associate, 大学院医学系研究科, 助手 (80314813)
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| Project Period (FY) |
2005 – 2006
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| Keywords | Brain edema / Brain ischemia / Fat emboli / Vascular endothelial growth factor / Astrocyte / Basal lamina |
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| Research Abstract |
The purpose of the present study was to examine the temporal profiles of astrocytic responses, water channel aquaporin 4(AQP4) and vascular endothelial growth factor(VGEF) in the process of brain edema formation in the fat embolism model in rat, comparing to those in focal brain ischemia. Brain water increased, reaching almost maximum at 2 h after intracarotid injection of triolein. Increased AQP4 immunostaining were observed in the peri-affected area but was absent in the core of the lesion 2h after triolein injection, and reactive astrocytes with hypertrophy and mitosis were observed 72h after triolein injection. VGEF immunostaining was also increased in astrocyte 2hr after triolein injection and was more significant 24h and 72h after triolein injection.
Basal lamina disappearance started to happen after 2h triolein injection and were more severe 24h and 72h after triolein injection. Neither significant increase of brain water content nor significant changes in AQP4 immunostaining were seen 2 h after MCAO. Our results indicate that AQP4, VGEF and basal lamina disappearance contribute to the brain edema formation of fat emboli. The modulation of these factors could lead the brain edema treatment.
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