1991 Fiscal Year Final Research Report Summary
Injury to plasma cell membrane after ischemia or hemorrhagic shock
| Project/Area Number |
02670543
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| Research Category |
Grant-in-Aid for General Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Research Field |
General surgery
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| Research Institution | Osaka University |
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Principal Investigator |
YOKOTA Junichiro Osaka University Medical School, Assistant, 医学部, 助手 (10166879)
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| Co-Investigator(Kenkyū-buntansha) |
YOSHIOKA Toshiharu Osaka University Medical School, Associate Professor, 医学部, 助教授 (60127313)
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| Project Period (FY) |
1990 – 1991
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| Keywords | Free radical / Superoxide dismutase / Catalase / Iron chelator / Endotoxin / カタラーゼ / 鉄キレート剤 / エンドトキシン |
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| Research Abstract |
We have previously reported that leukopenia or a combined treatment with superoxide dismutase (SOD) and catalase (CAT) can attenuate changes of membrane potential in postischemic skeletal muscle, and that free radical scavengers can diminish the persistent depolarization of cardiac and skeletal muscle cells following resuscitation from hemorrhagic shock.
In the first experiment of the current study, the effect of oxygen free radical scavengers (SOD+CAT) on blood flow, ATP content, and plasma cell membrane potential in the liver was evaluated after resuscitation from hemorrhagic shock. Oxygen free radical (OFR) -mediated cell membrane alteration was not noted in the lever, in contrast to cardiac and skeletal muscle. Pretreatment with scavengers, however, significantly improved portal vein blood flow and intestinal vessel blood flow. The results suggested that OFR-mediated alteration of the hepato-splanchnic circulation play an important role after hemorrhagic shock. In the second experiment, therefore, blood endotoxin was determined in the ischemia-reperfusion state of intestine. Significant endotoxemia was noted after declamping superior mesenteric artery. This study paved the way for the future study on bacterial translocation in the shock state. In the third experiment, to evaluate whether iron chelation with deferoxamine may interrupt postischemic skeletal muscle cell injury, tissue thiobarbituric acid reactive substances and membrane potential were measured during hind limb ischemia and after reperfusion. Pretreatment with iron chelator prevented lipid peroxidation and improved persistent depolarization of skeletal muscle cells.
Consequently, these studies yielded two significant results. Iron chelator as well as OFR scavengers can improve muscle cell membrane dysfunction induced after ischemia or shock. Intestinal injury after ischemia or shock may be mediated by OFR, and may be related to bacterial translocation.
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