1991 Fiscal Year Final Research Report Summary
The Role of Intracellular Ca^<2+> ion and Calmodulin in Organ Preservation
| Project/Area Number |
02454313
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| Research Category |
Grant-in-Aid for General Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Research Field |
Digestive surgery
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| Research Institution | University of Tokyo |
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Principal Investigator |
KAWANO Nobuhiro University of Tokyo, School of Medicine, 医学部(病), 講師 (40010160)
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| Co-Investigator(Kenkyū-buntansha) |
TSUKUI Hajime University of Tokyo, School of Medicine, 医学部(病), 医員 (90227380)
IZU Minoru University of Tokyo, School of Medicine, 医学部(病), 医員
ISHIMARU Masahiro University of Tokyo, School of Medicine, 医学部(病), 助手
GOTO Shin-ichiro University of Tokyo, School of Medicine, 医学部(病), 助手 (40186888)
OMORI Yoshimichi University of Tokyo, School of Medicine, 医学部(病), 医員 (60185395)
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| Project Period (FY) |
1990 – 1991
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| Keywords | liver ischemia / cirrhotic liver / Ca antagonist / calmodulin antagonist / intracellular Ca / NMR / 5FBAPTA / ATP |
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| Research Abstract |
Rat survival rate was examined after isolation of the liver with porto-jugular vein shunt. Survival rate was significantly increased both in normal liver rats and in liver cirrhosis rats after administering Ca++ antagonist and calmodulin antagonist. It was also found that reduction of ATP was accelerated after ischemia both in normal liver rats and in liver cirrhosis rats by administered calmodulin antagonist and Ca++ antagonist and that rat survival rate after reopening liver circulation was high in proportion to reduction rate of of ATP. These results were confirmed by both FIPLC and 31P-NMR method.
It is supposed that survival of the cell depends on the maintenance of potential difference across the cell membrane. We assumed that the cell which can effectively utilize ATP and maintain potential difference can resist ischemia. It was also assumed that Ca++ antagonist and calmodulin antagonist interrupt activation of phospholipase A2 and control the increase of intracellular FFA and then restrain hepatocellular damage caused by ischemia. This is because that intracellular FFA interrupt NaK ATPase and restrain the utilization of ATP. This was proved by measuring lactic acid and other parameters using 31P-NMR. But we could not measure the concentration of Ca++ ion accurately with NMR by administering rats 5FBAPTA. One of the reasons is that the magnetic field is weak and the other is that we cannot administer much dose because dissolvant of 5FBAPTA is much toxic. We could not measure intracellular Ca++ because fluorophotometer can measure 10-6 mol at most.
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Research Products
(6 results)
