1999 Fiscal Year Final Research Report Summary
Protection from and Treatment of Cerebrovascular Disturbances and Vascular Dementia by Angiogenesis
| Project/Area Number |
10671322
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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 |
Cerebral neurosurgery
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| Research Institution | Showa University |
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Principal Investigator |
FUJIMOTO Tsukasa Faculty of Medicine, Showa University, Professor, 医学部, 教授 (60014180)
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| Co-Investigator(Kenkyū-buntansha) |
SATO Tomoki Faculty of Pharmacology, Showa University, Assistant, 薬学部, 助手 (90183384)
ASAI Junichiro Faculty of Medicine, Showa University, Instructor, 医学部, 講師 (10151010)
SUZUKI Ryuta Faculty of Medicine, Showa University, Associate Professor, 医学部, 助教授 (10119216)
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| Project Period (FY) |
1998 – 1999
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| Keywords | ischemic cerebrovascular lesion / cerebral infarction / dura mater / indirect vascular reconstruction / angiogenesis / vascular dementia / vascular growth factor / VEGF |
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| Research Abstract |
Atheroscrelotic change is very important as a cause of cerebral thrombosis and vascular dementia. In 1992, we developed and have since used an indirect anastomosis, reversed durapexia (RDP), with which the ischemic brain gets effective neovessels, for surgical treatment of cerebral ischemia. We performed these experimental studies to make clear the mechanism of angiogenesis and to progress the RDP to more effective treatment. Four experiments were performed using rat ischemic model of which the middle cerebral artery was occluded. 1) Brains were removed periodically after the ischemic insult and were stained imuunohistochemically for growth factors, VEGF, bFGF and TGF-β. The expression of VEGF was strongest 7d after the ischemia, although expression was recognized from 1d to 30d. Both bFGF and TGF-βexpression was seen bilaterally but significant increase was recognized in the peripheral part of ischemic lesion from Id till 30d after the ischemic insult. Important roles for these factor
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s for angiogenesis at penumbra were suspected, 2) using same rat ischemic model, vascular density in 4 areas of each hemisphere was calculated using NIH image. Angiogenesis was significantly seen in the peripheral part of the infarct, strong expression of VEGF and continuous elevation of both growth factors was suspected of playing an important role in angiogenesis. This angiogenesjs might be important for repairing the infarcted area.
3) Similar rat ischemic model was used and following procedure was added. Namely, 2 lineal dural incisions were made on the dura mater which was coverling the ischemic brain, Fourteen days after the ischemia, significant angiogenesis from the surrounding dura mater to ischemic brain was induced. It was more significant than the angiogenesis from the surrounding brain tissue. 4) Similar model with experiment 3) was used and the combination of VEGF and bFGF was applied at the part of dural incision. Twenty-one days after the procedure, more significant angiogenesis than experiment 3) was recognized. This induced angiogenesis might be quite helpful for recover from and/or repairing of ischemic lesions. These results sujest the possibility that we might progress RDP to more effective method. Less
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