Defense mechanisms to increasing back pressure for hepatic oxygen transport and venous return in porcine fecal peritonitis.

High central venous pressure (CVP) acutely decreases venous return. How this affects hepatic oxygen transport in sepsis remains unclear. The aim of this study was to evaluate the effects of repeated increases in CVP via standard nursing procedures (NPs) on hepato-splanchnic and renal oxygen transport in a prolonged porcine sepsis model. Twenty anesthetized and mechanically ventilated pigs with regional hemodynamics monitored were randomized to fecal peritonitis or controls ( = 10 pigs/group). Resuscitation was started after 8 h of observation and continued for 3 days. NPs were performed at baseline and 8 h, 32 h, 56 h, and 72 h after resuscitation started. NPs increased CVP by 4-7 mmHg in both groups. In controls, this was associated with less decrease in hepatic arterial (Q; 62 ± 70 mL/min) than portal venous flow (Q; 364 ± 151 mL/min). Portal venous oxygen content and hepatic O delivery (Do) and consumption (V̇o) decreased by 11 ± 6 mL/dL and 0.9 ± 0.3 and 0.4 ± 0.3 mL·min·kg, respectively. In septic animals, hepatic Do decreased more in response to increasing CVP (1.5 ± 0.9 mL·min·kg), which was attributable to a larger fall in both Q (88 ± 66 ml/min) and portal O content (14 ± 10 mL/dL, all < 0.05). This resulted in numerically lower hepatic V̇o since O extraction did not increase significantly. In control conditions, a smaller decrease in Q compared with Q helped to limit the reduction in hepatic V̇o in response to acute CVP increase. In sepsis, the contribution of Q to maintain hepatic Do was reduced, which jeopardized hepatic V̇o further. Renal arterial flow was similarly affected by CVP increase as Q. Sepsis impairs intrinsic mechanisms to attenuate effects of increasing back pressure on hepatic oxygen transport.