| Project/Area Number |
17590741
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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 |
Circulatory organs internal medicine
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| Research Institution | Kagawa University |
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Principal Investigator |
OHMORI Koji Kagawa University, Faculty of Medicine, Associate Professor (00263913)
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| Co-Investigator(Kenkyū-buntansha) |
KOHNO Masakazu Kagawa University, Faculty of Medicine, Professor (20153489)
SHINOMIYA Kaori Kagawa University, Faculty of Medicine, Assistant Professor (70380160)
TAKEUCHI Hiroto Kagawa University, Faculty of Medicine, Assistant Professor (90372721)
松本 義人 香川大学, 医学部, 助手 (80311827)
藤田 憲弘 香川大学, 医学部, 助手 (40322268)
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| Project Period (FY) |
2005 – 2006
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| Project Status |
Completed (Fiscal Year 2006)
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| Budget Amount *help |
¥3,500,000 (Direct Cost: ¥3,500,000)
Fiscal Year 2006: ¥1,000,000 (Direct Cost: ¥1,000,000)
Fiscal Year 2005: ¥2,500,000 (Direct Cost: ¥2,500,000)
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| Keywords | microbubble / ultrasound / angiogeriesis / leukocyte / granulocvte colony stimulating factor / collateral vessel / acoustic pressure / 顆粒球コロニー刺激因子 / 炎症 / 超音波診断 / 粥腫 |
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| Research Abstract |
Activity of atheroma plaque depends on the severity of ongoing inflammation. Therefore, we applied contrast ultrasound to inflammation imaging. We obtained images of kidneys by diagnostic ultrasound pressure after suspension of ultrasound emission for 10 minutes allowing phagocytosis of microbubbles (MB) by leukocytes following MB injection. By subtracting perfusion image from this image, we extracted signals from retained (phagocytosed) MB. The signal distributed in the medulla in the ischemia reperfusion model and in the cortex in the glomerulonephritis model, which well agreed with the distribution of leukocytes in respective models. We applied this imaging method to mouse hindlimbs ischemia model of hypoperfused-inflamed tissue that better mimics atheroma plaque. The similar settings provided an opacification that represents retained MB. Thus, using ordinary acoustic pressure we can image retained microbubbles in the inflamed tissue by devising timing. However, histological assessm
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ent of its safety revealed that leukocyte infiltration was aggravated after 24 hours of imaging, which was unfavorable side effect potentially causing plaque rupture. In order to avoid this side effect a low-acoustic pressure apparatus with advanced sensitivity needs to be devised in the future. However, the side effect causing leukocyte infiltration could be applicable to therapeutic angiogenesis, because leukocytes release vascular endothelial growth factor and granulocyte colony stimulating factor (G-SF) has been used in therapeutic angiogenesis. We applied this method to the same model and found that it significantly further augmented angiogenesis in combination with pre-administration of 300 microgram G-CSF which was minimum effective dose at monotherapy. Thus, inflammation imaging by contrast ultrasound using current apparatus can evaluate leukocyte infiltration or activity of inflammation which determine the severity of respective pathology, but aggravated inflammation. However, this side effect was applicable to enhancement of therapeutic angiogenesis which would be worth while optimizing in the future study. Less
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