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Continuous infusion of prostaglandin E1 via the superior mesenteric artery can prevent hepatic injury in hepatic artery interruption through passive portal oxygenation
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Abstract: Aims/Background: Hepatic artery interruption (HAI) causes severe ischemic liver damage, especially following hepatopancreatobiliary surgery. In order to inhibit a decrease in oxygen delivery after HAI, continuous infusion of PGE1 via the superior mesenteric artery (SMA) was administered in pigs and changes in hepatic blood flow and oxygen delivery were investigated. Furthermore, its effectiveness in the prevention of liver injury was evaluated by histology and serum enzyme levels. Methods: Animals were subjected to HAI without PGE1 infusion (control group n=6) and to continuous infusion of PGE1 (0.02 μg/kg/min) into the SMA (PGE1 group n=6). Results and Conclusion: PGE1 infusion via the SMA not only increased the portal blood flow but also elevated the oxygen content of the portal blood. The reduction in oxygen delivery to the liver was 50% in the control group, and only 13% in the PGE1 group. Serum aspartate aminotransferase (AST) and lactate dehydrogenase (LDH) levels 24 h after HAI in the control group were 3415±1283 IU/L and 9839±2959 respectively while in the PGE1 group they were 939±426 IU/L and 5510±1545 IU/L respectively. Histological examination showed massive necrosis in the control group at 72 h but only focal liver cell necrosis in the PGE1 group. Based on this finding and the fact that this treatment can be performed easily and safely, continuous infusion of PGE1 via the SMA may be a useful intervention to prevent severe liver damage after hepatic artery interruption.
Title: Continuous infusion of prostaglandin E1 via the superior mesenteric artery can prevent hepatic injury in hepatic artery interruption through passive portal oxygenation
Description:
Abstract: Aims/Background: Hepatic artery interruption (HAI) causes severe ischemic liver damage, especially following hepatopancreatobiliary surgery.
In order to inhibit a decrease in oxygen delivery after HAI, continuous infusion of PGE1 via the superior mesenteric artery (SMA) was administered in pigs and changes in hepatic blood flow and oxygen delivery were investigated.
Furthermore, its effectiveness in the prevention of liver injury was evaluated by histology and serum enzyme levels.
Methods: Animals were subjected to HAI without PGE1 infusion (control group n=6) and to continuous infusion of PGE1 (0.
02 μg/kg/min) into the SMA (PGE1 group n=6).
Results and Conclusion: PGE1 infusion via the SMA not only increased the portal blood flow but also elevated the oxygen content of the portal blood.
The reduction in oxygen delivery to the liver was 50% in the control group, and only 13% in the PGE1 group.
Serum aspartate aminotransferase (AST) and lactate dehydrogenase (LDH) levels 24 h after HAI in the control group were 3415±1283 IU/L and 9839±2959 respectively while in the PGE1 group they were 939±426 IU/L and 5510±1545 IU/L respectively.
Histological examination showed massive necrosis in the control group at 72 h but only focal liver cell necrosis in the PGE1 group.
Based on this finding and the fact that this treatment can be performed easily and safely, continuous infusion of PGE1 via the SMA may be a useful intervention to prevent severe liver damage after hepatic artery interruption.
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