1993 Fiscal Year Final Research Report Summary
Protective effect of immunosuppressants on ischemia and reperfusion injury in the liver
| Project/Area Number |
04670784
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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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| Research Field |
消化器外科学
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| Research Institution | Kagawa Medical School |
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Principal Investigator |
MAEBA Takashi Kagawa Medical School, School Hospital, Assistant Professor, 医学部・附属病院, 講師 (60157154)
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| Co-Investigator(Kenkyū-buntansha) |
WAKABAYASHI Hisao Kagawa Medical School, Medical School, Senior Fellow, 医学部, 助手 (60240446)
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| Project Period (FY) |
1992 – 1993
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| Keywords | liver / 31P-MRS / ischemia and reperfusion / ICAM-1 / FK506 |
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| Research Abstract |
The protective effect of FK 506 on hepatocytes against ischemia and reperfusion injury was examined by evaluating the followings : the high energy phosphorus metabolism obtained by using 31P-MRS (magnetic Resonance Spectroscopy) and tissue blood flow of the liver in ischemia and reperfusion process, m-GOT and GPT, survival rates of the animals and histological study and immunohistological staining for ICAM-1 in the liver after ischemia. The rats were treated with FK506 (1mg/kg/day) by intramuscular injection for 4 days before testing. Ischemia was induced by clamping the hepatoduodenal ligament for 30 minutes. In 31P-MRS, the recovery of hepatic energy status after ischemia, evaluated by beta-ATP/inorganic phosphate (Pi), was significantly better in the FK506 group. Itcoinsided with the recovery of tissue blood flow monitored by laser Doppler flow meter. On histological examination, congestion observed in the periportal region of the control group was mild, while there was less induction of ICAM-1 on endothelial cells of the portal veins and hepatic veins in the FK506 group. Upon these findings we concluded that FK506 had a protective effect on hepatocytes against warm ischemia and reperfusion injury, and part of its mechanism could be attributed to improvement of tissue blood flow after ischemia by the modulation of immunological events.
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