| Budget Amount *help |
¥2,100,000 (Direct Cost: ¥2,100,000)
Fiscal Year 1990: ¥300,000 (Direct Cost: ¥300,000)
Fiscal Year 1989: ¥1,800,000 (Direct Cost: ¥1,800,000)
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| Research Abstract |
The purpose of this study is to clarify the limit of reperfusion inJuries in the liver and the changes of prostanoid and endotoxin in the blood or lipid peroxidative reaction by interrupting not only hepatic blood inflow but also that in the hepatic inferior vena cava, using adult mongrel dogs. The experimental models were classified into 3 groups:GroupI (60-minute ischemia), GroupII (120-minute ischemia) and GroupIII (GroupII+liver perfusion with 4^ﾟC Ringer's solution). During interruption of blood flow in the hepatic artery, portal vein, and both superior and inferior hepatic portionof inferior vena cava, stasis blood in the portal vein and inferior vena cava were bypassed into the jugular vein using a blood delivery pump。 For perfusion, a catheter for ischemic liver flashing was inserted into the main portal vein toward the liver side and a catheter for drainage of fluid perfused from liver into the hepatic inferior vena cava via the femoral vein. 1. The survival rate of 5 days aft
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er reperfusion was 83% in Group I, 14% in GroupII, and 43% in GroupIII, and liver failure was the main cause of death in all non-survivors. 2。 Liver function was impared immediately after reperfusion in each group and normalized at 3days after reperfusion in the survivors but aggravated in the non-survivors. GorupII showed the most marked abnormality in liver function, comparing with Groups I andIII. 3. Prostanoid in blood : 6-keto-prostaglandin-F_<1alpha> (6KF) increased immediatelyafter reperfusion, and it showed highest value in GroupII. 6KF was decreased markedly after 3hours in the survivors of GroupI and II. On the other hand, thromboxane B_2(TxB_2 was high in the survivors but rapidly decresed 3hours after reperfusion in the non-survivors. Therefore TxB_2/6-KF was marked low value immediately after reperfusion in GroupII shown poorest prognosis. 4. Blood endotoxin increased after reperfusion in each group, reaching a peak after 3hours, but decreased thereafter ; the recovery in GroupII was significantly delayed. 5. Blood lipid peroxide was high after reperfunsion but was normalized after 3days in the survivors, being correlated with the lipid peroxide concertration in the liver. 6. Blood flow in the liver tissue decreased 2hours after reperfusion and recovered in the survivors. In sinusoids of the liver, Kupffer cell hyertrophy was observed even after 7days but improved by after 14days.
These findings provide useful information on the limit and reversibility of ischemia in the liver. Less
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