gms | German Medical Science

Introduction: Liver resection with median hepatic vein (MHV) transsection may result in a focal outflow obstruction (FOO). FOO can reduce the functional liver mass and cause a "small-for-size" liver syndrome.

In our group, a surgical rat model of FOO has been developed by Dr. Dirsch. In this model, the right MHV is ligated, which impairs the blood outflow of liver. We demonstrated that these canals expressed vascular markers (vW and FVIII) indicative of a vascular remodeling process (VRP) from multiple dilated sinusoids to formation of single VC.

Aim of this study was to visualize VRP on a macroscopical scale and relate morphological findings to underlying molecular events.

Materials and methods: FOO was induced by ligating RMHV in male Lew rats. Rats were sacrificed at 0h, 24h, 48h and 1 week post-op and one liver was injected retrogradely via superior cava with polymer (Batson kit) prior to digesting the hepatic parenchyma using KOH. The corrosion casts were subjected to Dual-Energy-CT and subsequent 3D-reconstruction using of Mevis software.

Results: After RMHVL, only the stump of RMHV could be filled with the polymer. The main tree of RMHV was not filled and appeared as a “hole” in hepatic venous corrosion cast. Within one week, RMHV-tree reappeared, although the stump at the site of ligation was still visible as such. SVC with a minimal diameter of 11µm connecting RMHV-territory with middle MHV territory presumably draining the hepatic inflow from RMHV-territory into MMHV territory. Formation of the macroscopically visible VC was preceded by expression of vascular marker in the dilated sinusoids indicative of vascularisation process. VC formation was paralleled by the complete absorption of the confluent necrosis within the obstructed lobe. Figure 1 [Fig. 1].

Conclusion: This imaging study visualizes the kinetics of VRP leading to complete restoration of hepatic venous drainage in parallel with resorption of confluent necrosis after an acute FOO.