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Background. Hepatic ischemia–reperfusion (I/R) is accompanied by liver weight gain and ascites formation. This could be caused by an increase in sinusoidal pressure, a determinant of hepatic transvascular fluid movement. We determined the role of sinusoidal pressure, assessed by triple vascular occlusion pressure (Pto), in the I/R injury in isolated rat livers perfused with leukocyte-free diluted blood bivascularly via the portal vein and hepatic artery.
Materials and methods. Ischemia was induced at room temperature by occlusion of either the inflow lines of the hepatic artery and portal vein (the open outflow group, n = 10) or both the inflow and the outflow (hepatic venous) lines (the closed outflow group, n = 10) for 1 h, followed by 1-h reperfusion in a recirculating manner.
Results. Liver weight in both groups increased biphasically after reperfusion; the initial peak occurred at 3 min and the second peak at 60 min. Immediately after reperfusion, Pto peaked, followed by a gradual decline. The initial weight increase in groups combined was significantly and positively correlated with an increase in Pto (r = 0.716, P = 0.0002), but the second peak was independent of Pto. Liver injury, assessed by perfusate levels of hepatic enzymes and reduced bile flow rate, was observed at 60 min after reperfusion in both groups.
Conclusions. These findings suggest that increased sinusoidal pressure contributes to only the early liver weight gain after reperfusion in isolated perfused rat livers. The late weight gain may be presumably due to liver injury.
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☆This study was supported by Grant-in-Aid for Scientific Research 10557138 from the Ministry of Education, Science, and Culture of Japan.
© 2000 Academic Press. Published by Elsevier Inc. All rights reserved.