| Project/Area Number |
07671654
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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 | Nagoya University |
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Principal Investigator |
MIKE Norio Nagoya University School of Medicine, Anesthesiology, Assistant Professor, 医学部, 助手 (20192354)
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| Co-Investigator(Kenkyū-buntansha) |
FUJIWARA Yoshihiro Nagoya University School of Medicine, Anesthesiology, Assistant Professor, 医学部, 助手 (70238640)
KIMURA Tomomasa Nagoya University School of Medicine, Anesthesiology, Assistant Professor, 医学部, 講師 (50161568)
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| Project Period (FY) |
1995 – 1996
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| Project Status |
Completed (Fiscal Year 1996)
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| Budget Amount *help |
¥2,300,000 (Direct Cost: ¥2,300,000)
Fiscal Year 1996: ¥1,200,000 (Direct Cost: ¥1,200,000)
Fiscal Year 1995: ¥1,100,000 (Direct Cost: ¥1,100,000)
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| Keywords | adhesion molecules / endothelial cell / open heart surgery / hepatic surgery / allograft cell / CD11a / CD18 |
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| Research Abstract |
Extracorporeal circulation reduces leucocyte activation and leucocyte adhesion-related phenomena. The expression of the adhesion molecules CD11 and CD18 which mediated inflammation and allograft rejection were examined in the patients with open heart surgery. We obtained leukocyte at the point of preoperative period and intraoperative period. We analyzed antigen expression of leukocyte using flowcytometry with monoclonal antibodies to CD11 and CD18. Extracorporeal circulation reduced the expression of CD11 and CD18 on leucocyte. Cellular adhesion molecules are, thus, important in would healing and other inflammatroy process relevant to open heart surgery.
In addition, we analyzed gene polymorphism of angiotensin converting enzyme using molecular biological technique in patients with neuropathic pain. DD genotype which relevant cardiovascular complications showed 33% of all patients which means higher incidence than the incidence of the patients without pain. These results indicated the genetic factor of neuropathic pain.
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