| Project/Area Number |
09045080
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| Research Category |
Grant-in-Aid for international Scientific Research
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| Allocation Type | Single-year Grants |
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| Section | University-to-University Cooperative Research |
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| Research Field |
Digestive surgery
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| Research Institution | KYOTO UNIVERSITY |
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Principal Investigator |
YAMAMOTO Yuzo Kyoto UNiv. Graduate School of Med. Instructure, 医学研究科, 助手 (70281730)
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| Co-Investigator(Kenkyū-buntansha) |
YAMAOKA Yoshio Kyot Univ. Graduate School of Med. Professor, 医学研究科, 教授 (90089102)
HAMMER Claus Univ. Munich Int. for Surg. Research. Professor, 実験外科学研究所, 教授
MESSMER Konard Univ. Munich Int. for Surg. Research .Professor, 実験外科学研究所, 教授
OZAKI Nobuhiro Kyoto UNiv. Graduate School of Med. Instructure, 医学研究科, 助手 (50211818)
MESSMER Konr ミュンヘン大学, 実験外科学研究所, 教授
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| Project Period (FY) |
1997
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| Project Status |
Completed (Fiscal Year 1997)
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| Budget Amount *help |
¥2,400,000 (Direct Cost: ¥2,400,000)
Fiscal Year 1997: ¥2,400,000 (Direct Cost: ¥2,400,000)
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| Keywords | stress protein / Brain-Death / Liver Transplantation / Hepatic Microcirculation / Ischemia-Reperfusion / Tolerance / Cushing Phenomenon / Adhesion Molecule |
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| Research Abstract |
Brain-dead model of rats was established in this research. Electro-encephalogram became reduced 2-3 minutes after induction of brain-death and it was completely flat at 1-3 hours during brain-dead state. Corneal reflex was disappeared. Blood pressure showed a steep elevation upon the increase of intracranial pressure and then rapidly decreased. Stable low blood pressure continued thereafter at least for 3 hours. The criteria of brain-death was fulfilled. Concerning the microcirculation of the liver, adhesion of leukocytes to sinusoidal endothelium was increased and the calibers of the portal vein and post-sinusoidal vessels were smaller in the brain-dead model. The flow rate of leukocytes was remarkably decreased. Expression of CD11 of leukocytes was significantly enhanced in the brain-death. These results were not consistent with the speculation of maintained hepatic microcirculation during brain-dead state due to alpha stimulation blockade, which was supposed from the highly maintain
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ed arterial ketone body ratio in the brain-dead model of dogs. However, the hepatic energy metabolism is once discontinued during cold preservation after procurement from brain-dead state aid is restarted upon blood reperfusion after transplantation. It is therefore possible that the deterioration of microcirculation due to activation of some cytokines during brain-death results only in the latent harm of the liver function, i. e. in the range of hepatic functional reserve, and the damage become overt after cold ischemia and reperfusion to produce primary graft dysfunction. As for production of heat shock proteins during brain-death, HSP72 protein was not detected by Western-blot, probably because of short period of 3 hours after the onset of brain-death. Concerning the m-RNA of HSP72, even the sham operated animal expressed it. This is why the effects of Cushing phenomenon to trigger the HSP72 expression could not be fully determined in this study period. The analyses of special microenvironment in which the brain-dead graft is maintained and those of the stress response at cellular level in the brain-dead state will enable us to manipulate the stress response in the brain-dead liver so that we can develop a new molecular surgery to improve liver transplantation. Less
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