Portal hyperperfusion after major liver resection and associated sinusoidal damage is a therapeutic target to protect the remnant liver.

Extended liver resection results in the loss of a large fraction of the hepatic vascular bed and thereby abrupt alterations in the perfusion of the remnant liver. Mechanisms of hemodynamic adaptation and associated changes in oxygen metabolism after liver resection and the effect of mechanical portal blood flow reduction were assessed. A pig model (n=16) of extended partial hepatectomy that included continuous observation for 24 hours under general anesthesia was established. Pigs were randomly separated into 2 groups, one group with a portal flow reduction of 70% compared to the preoperative values, and the other group as a control (n=8, each). In controls, portal flow [mean (SD)] increased from 74 (8) (ml/min)/100g preoperatively to 240 (48) (ml/min)/100g at 6 hours after resection (p<0.001). Hepatic arterial buffer response was abolished after resection. Oxygen uptake per unit liver mass increased from 4.0 (1.1) (ml/min)/100g preoperatively to 7.7 (1.7) (ml/min)/100g 8 hours after resection (p=0.004). Despite this increase in relative oxygen uptake, total hepatic oxygen consumption was not maintained and markers of hypoxia and anaerobic metabolism were significantly increased in hepatocytes after resection. Reduced postoperative portal flow was associated with significantly decreased levels of aspartate aminotransferase and bilirubin and increased hepatic clearance of indocyanine green. In conclusion, major liver resection was associated with persistent portal hyperperfusion, loss of the hepatic arterial buffer response, decreased total hepatic vO2 and with increased anaerobic metabolism. Portal flow modulation by partial portal vein occlusion attenuated liver injury after extended liver resection.