2005 Fiscal Year Final Research Report Summary
An experimental study on resuscitation of tissue dysoxia
| Project/Area Number |
16591809
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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 |
Emergency medicine
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| Research Institution | Hamamatsu University School of Medicine |
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Principal Investigator |
AOKI Katsunori Hamamatsu University School of Medicine, Professor, 医学部, 教授 (20124927)
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| Co-Investigator(Kenkyū-buntansha) |
MAGATA Yasuhiro Hamamatsu University School of Medicine, Photon Medical Center, Professor, 光量子医学研究センター, 教授 (20209399)
YOSHINO Atsuto Hamamatsu University School of Medicine, Associate Professor, 医学部, 助教授 (00262816)
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| Project Period (FY) |
2004 – 2005
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| Keywords | dysoxia / shock / tissue oxygen metabolism / iluem / Pd-porphrin / arteriovenous shunt / endotoxin |
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| Research Abstract |
The purpose of this study was to evaluate tissue dysoxia in an experimental model of hemorrhagic shock and endotoxin shock. Ten rabbits (Japan White Rabbits, BW 3kg) were assigned to 2 groups. Group A (n=5) was resuscitated by blood transfusion and Group B (n=5) by isotonic crystalloid solution. The value of ileum serosal oxygen partial pressure was about 30 mmHg lower by the method of Pd-porphyrin phsophorescense than by the method of the oxygen electrodes. The reason why the two methods provided different data was that Pd-porphyrin phsophorescense measured the tissue oxygen pressure in the deeper layer of ileum than the oxygen electrode. The value of ileum serosal oxygen partial pressure decreased in hemorrhagic shock and showed lower than the value of venous oxygen partial pressure. This gap of oxygen partial pressure between tissue and vein was apparently seen in the group resuscitated by crystalloid solution. This shunt effect seen in the hemorrhagic shock was significantly prevented with hyperoxia. On the other hand, a decrease in ileal serosal oxygen partial pressure and persistent negative oxygen gap between tissue and vein was seen in endotoxin shock model induced by LPS(Escherichia coli-055:B5, mg/kg) in 10 animals. We conclude that tissue dysoxia may form at an early stage in hemorrhagic shock and endotoxin shock and shunting of the microcirculation may be an important contributing factor to development of multiple organ failure. To evaluate the severity of the shunting effect, new technologies aimed at the microcirculation will need to be developed about analysis of heterogenous distribution of oxygen in tissue.
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