Effect of endotoxemia on hepatic portal and sinusoidal blood flow in rats

A decrease of liver blood flow leads to a dysfunction of hepatocytes and Kupffer-cells with subsequent local and systemic liberation of proinflammatory mediators [1] that may maintain SIRS and may lead to MODS [2]. There is only limited knowledge about the hepatic micro- and macrocirculation during sepsis or endotoxemia. Therefore, aim of our study was to investigate alterations in hepatic portal (PBF) and sinusoidal blood flow (SBF) during endotoxemia.

In male Wistar rats endotoxemia was induced by continuous infusion of 2 mg/kg/h lipopolysaccharides (LPS) from E. coli 026:B6 immediately after baseline measurements (LPS group; n = 10). The control group (n = 10) received an equivalent volume of Ringer's solution. MAP, HR, CO, PBF and SBF were measured at baseline, and 60 min, and 120 min after induction of endotoxemia. PBF was measured using a laser-doppler flow probe that was positioned around the portal vein. SBF was detected by in vivo videomicroscopy of the left liver lobe. Statistical analysis was performed using Mann-Whitney's U-test.

MAP and CO remained at baseline values in both groups. In the LPS-group HR significantly increased. During endotoxemia PBF and SBF significantly decreased (Table).

Our results demonstrate that during early endotoxemia hepatic macro- and microcirculatory perfusion is significantly decreased despite unchanged MAP and CO. This early reduction of hepatic perfusion might be caused by an increased hepatic vessel resistance as a consequence of liberation of vasoconstrictive mediators (e.g. endothelin) or/and by a decrease in intestinal perfusion.

Table Our results demonstrat