| Budget Amount *help |
¥4,940,000 (Direct Cost: ¥3,800,000、Indirect Cost: ¥1,140,000)
Fiscal Year 2015: ¥260,000 (Direct Cost: ¥200,000、Indirect Cost: ¥60,000)
Fiscal Year 2014: ¥780,000 (Direct Cost: ¥600,000、Indirect Cost: ¥180,000)
Fiscal Year 2013: ¥3,900,000 (Direct Cost: ¥3,000,000、Indirect Cost: ¥900,000)
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| Outline of Final Research Achievements |
This study was conducted to clarify the mechanisms for perioperative modulation of albumin permeability across endothelial cell monolayers. The expression of mRNA for full-length neurokinin-1 receptor NK1R in endothelial cells was confirmed although the level of expression was very low. The level of mRNA for truncated NK1R was much higher and constitutive. A NK1R ligand substance P (SP), failed to modulate the albumin permeability when it was solely applied, while it accelerated the permeability in combination with fresh frozen plasma (FFP). The increase in the albumin permeability by FFP was potently blocked by reagents with anti-thrombin activities (heparin or urinastatin). A NK1R antagonist Spantide reduced the FFP-provoked albumin permeability even in the absence of SP added. Endothelial cells expressed the mRNA for hemokinin (TAC4), indicating that hemokinin/NK1R pathway may be involved in the autocrine regulation for endothelial cell functions.
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