Liu, Shengchen; Kohler, Andreas; Langer, Rupert; Jakob, Manuel O; Salm, Lilian; Blank, Annika; Beldi, Guido; Jakob, Stephan M (2022). Hepatic blood flow regulation but not oxygen extraction capability is impaired in prolonged experimental abdominal sepsis. American journal of physiology - gastrointestinal and liver physiology, 323(4), G348-G361. American Physiological Society 10.1152/ajpgi.00109.2022
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Impaired oxygen utilization has been proposed to play a significant role in sepsis-induced liver dysfunction, but its magnitude and temporal course during prolonged resuscitation is controversial. The aim of this study is to evaluate the capability of the liver to increase oxygen extraction in sepsis during repeated acute portal vein blood flow reduction. Twenty anesthetized and mechanically ventilated pigs with hepatic hemodynamic monitoring were randomized to fecal peritonitis or controls (n=10, each). After 8-hour untreated sepsis, the animals were resuscitated for three days. The ability to increase hepatic O2 extraction was evaluated by repeated, acute decreases in hepatic oxygen delivery (DO2) via reduction of portal flow. Blood samples for liver function and liver biopsies were obtained repeatedly. While liver function tests, ATP content, and hepatic oxygen delivery (DO2) remained unaltered, there were signs of liver injury in blood samples and overt liver cell necrosis in biopsies. With acute portal vein occlusion, hepatic DO2 decreased more in septic animals compared to controls (max. decrease: 1.66±0.68 ml/min/kg in sepsis vs. 1.19±0.42 ml/min/kg in controls; Qpv reduction-sepsis interaction: p=0.028). Hepatic arterial buffer response (HABR) was impaired, but recovered after 3-day resuscitation, while hepatic oxygen extraction increased similarly during the procedures in both groups (max. increase: 0.27±0.13 in sepsis vs. 0.18±0.09 in controls; all p>0.05). Our data indicates maintained capacity of the liver to acutely increase O2 extraction, while blood flow regulation is transiently impaired with the potential to contribute to liver injury in sepsis.
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