Intrahepatic Tissue pO2 during Continuous or Intermittent Vascular Inflow Occlusion in a Pig Liver Resection Model

Abstract

Background: Temporary vascular inflow occlusion of the liver (clamping of the hepatic pedicle) can prevent massive blood loss during liver resections. In this study, intrahepatic tissue pO₂ was assessed as parameter of microcirculatory disturbances induced by ischemia and reperfusion (I/R) in the liver following continuous (Cnt) or intermittent (Int) clamping in a hemihepatectomy model in the pig. Methods: Pigs (20–34 kg) were divided into 2 groups: I/R without hemihepatectomy (–HH; n = 10) and I/R with hemihepatectomy (+HH; n = 8). Ischemia during 90 min was Cnt or Int (6 sequential periods of 12 min of ischemia and 3 min of reperfusion), followed by 120 min of reperfusion. Intrahepatic pO₂ histograms (polarographic pO₂ needle electrode) were constructed before ischemia, at the end of 90 min of ischemia and after 120 min of reperfusion, along with assessment of plasma AST, ALT and LDH. Bile production was monitored continuously. Results: Cumulative frequency distribution curves (CFDC) after 120 min of reperfusion in the Cnt–HH group were not different from preischemic CFDC (means ± SEM), whereas in the Int–HH group a left shift occurred indicating more hypo(non)perfused liver areas (pO₂ < 10 mm Hg: 2.6 ± 1.2 and 41.0 ± 17.5% in Cnt–HH and Int–HH; p < 0.01). In the Cnt+HH group, a left shift in the CFDC occurred. In the Int+HH group, a left and a right shift occurred simultaneously, indicating both hypo(non)- and hyperperfused (shunting) liver areas (pO₂ < 10 mm Hg: 4.0 ± 2.7 and 9.6 ± 8.5%, n.s., and pO₂ > 60 mm Hg: 2.0 ± 2.0 and 17.3 ± 6.4%, p = 0.015, in Cnt+HH and Int+HH). Plasma AST, ALT and LDH levels were not increased after 120 min of reperfusion, except for AST in Cnt+HH and Int+HH (from 54.6 ± 14.0 to 270.4 ± 42.8 U/l, p < 0.01, and from 47.8 ± 9.4 to 176.5 ± 55.9 U/l, n.s.). Bile production (percentage of mean preischemic value) during 120 min of reperfusion was significantly reduced in the Int–HH group, as compared to the Cnt–HH group (57.0 and 117.0% after 120 min of reperfusion, p = 0.002). In Cnt+HH and Int+HH, bile production was significantly reduced (33.3 ± 20.0%, p = 0.05, and 38.5 ± 7.9%, p = 0.007); however it was not different between the two groups. Conclusions: (1) Intrahepatic tissue pO₂ as indicator of microvascular perfusion is a parameter of early I/R injury; (2) continuous vascular inflow occlusion resulted in less microcirculatory disturbances, when compared to intermittent occlusion.