2000 Fiscal Year Final Research Report Summary
Endovascular photodynamic therapy to inhibit intimal hyperplasia
| Project/Area Number |
11671186
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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 |
General surgery
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| Research Institution | Tokyo Medical University |
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Principal Investigator |
NAGAE Tsuneyuki M.D., Tokyo Medical University, Department of Medicine Assistant Professor of Surgery, 医学部, 講師 (70217967)
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| Co-Investigator(Kenkyū-buntansha) |
AIZAWA Katsuo Ph.D., Tokyo Medical University, Department of Physiology, Professor of Physiology, 医学部, 教授 (40074645)
ISHIMARU Shin M.D., Tokyo Medical University, Department of Surgery, Professor of Surgery, 医学部, 教授 (50112785)
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| Project Period (FY) |
1999 – 2000
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| Keywords | photodynamic therapy / Intimal hyperplasia / restenosis |
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| Research Abstract |
Photodynamic therapy reportedly inhibits the development of intimal hyperplasia. In this study, we examined time-course arterial accumulation and distribution of a second generation photosensitizer mono-l-aspartyl chlorin e6 (NPe6) in rabbit arterial models. Arterial NPe6 concentration was measured by HPLC and epifluorescence of NPe6 was observed by our developed epifluorescence image analysis system. The peak values of NPe6 concentration in balloon injured arteries and atherosclerotic arteries were significantly high when compared with the normal arteries.
For homogeneous radial laser irradiation to the vessel wall, we used newly developed cylindrical diffusing balloon laser fiber. Injuries were induced by pulling a balloon catheter through the right iliac artery of rabbits. The arteries were harvested at two days and 2 weeks.
Endovascualr NPe6-PDT showed complete depletion of smooth muscle cells using low-dose laser at 2 days. Intimal hyperplasia was significantly inhibited at 2 weeks after PDT.Endovascular PDT of injured artery using NPe6 can inhibit intimal hyperplasia in this experimental model and may be effective in inhibiting to form hyperplastic lesions after arterial interventions.
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