BACKGROUND/AIMS: We have proposed that acute portal hypertension, reflecting sinusoidal shear stress, becomes a trigger of liver regeneration after partial hepatectomy. Moreover, excessive shear stress induces liver injury. We investigated whether the use of a portosystemic shunt can reduce surplus damage of the remnant liver by means of excessive shear stress after massive hepatectomy. METHODOLOGY: In this study, to determine whether and by what mechanism excessive shear stress induces liver injury, we used the rat model to investigate whether a subcutaneous splenic transposition, which consists of a portosystemic shunt up to 4 weeks post-surgery, can prevent liver injury. RESULTS: Subcutaneous splenic transposition decreased the portal pressure immediately after 90% massive hepatectomy and relieved the elevation of transaminase and serum hyaluronic acid compared with findings of the no shunt group. In addition, the degree of leukocytopenia and thrombocytopenia in 90% massive hepatectomy with subcutaneous splenic transposition were better than those in 90% massive hepatectomy without subcutaneous splenic transposition. Serum tumor necrosis factor-alpha levels of the shunt group were lower than those of massive hepatectomy without subcutaneous splenic transposition. The rats that underwent 95% massive hepatectomy died within 48 hrs. The extent to which subcutaneous splenic transposition prolonged survival after 95% massive hepatectomy was statistically significant (mean survival of shunt group 60.9 +/- 13.4 hours vs. no shunt group 25.4 +/- 2.3 hours P = 0.001). CONCLUSIONS: These findings suggest that excessive shear stress after massive hepatectomy induces the liver injury against the hepatocytes and the sinusodial endothelial cells via intrahepatic microcirculation failure accompanied by overimmunoreaction.
BACKGROUND/AIMS: We have proposed that acute portal hypertension, reflecting sinusoidal shear stress, becomes a trigger of liver regeneration after partial hepatectomy. Moreover, excessive shear stress induces liver injury. We investigated whether the use of a portosystemic shunt can reduce surplus damage of the remnant liver by means of excessive shear stress after massive hepatectomy. METHODOLOGY: In this study, to determine whether and by what mechanism excessive shear stress induces liver injury, we used the rat model to investigate whether a subcutaneous splenic transposition, which consists of a portosystemic shunt up to 4 weeks post-surgery, can prevent liver injury. RESULTS: Subcutaneous splenic transposition decreased the portal pressure immediately after 90% massive hepatectomy and relieved the elevation of transaminase and serum hyaluronic acid compared with findings of the no shunt group. In addition, the degree of leukocytopenia and thrombocytopenia in 90% massive hepatectomy with subcutaneous splenic transposition were better than those in 90% massive hepatectomy without subcutaneous splenic transposition. Serum tumor necrosis factor-alpha levels of the shunt group were lower than those of massive hepatectomy without subcutaneous splenic transposition. The rats that underwent 95% massive hepatectomy died within 48 hrs. The extent to which subcutaneous splenic transposition prolonged survival after 95% massive hepatectomy was statistically significant (mean survival of shunt group 60.9 +/- 13.4 hours vs. no shunt group 25.4 +/- 2.3 hours P = 0.001). CONCLUSIONS: These findings suggest that excessive shear stress after massive hepatectomy induces the liver injury against the hepatocytes and the sinusodial endothelial cells via intrahepatic microcirculation failure accompanied by overimmunoreaction.