gms | German Medical Science

Introduction: Focal hepatic venous outflow obstruction occurs frequently when MHV is transected, as done in extended hepatectomy. We previously observed that focal hepatic venous outflow obstruction could recover spontaneously after right median hepatic vein (RMHV) ligation+partial hepatectomy (PH) in rats via formation of vascularized sinusoidal canals (VSC). According to the hepatic arterial buffer response theory, portal hypertension after PH causes a reduction of hepatic arterial perfusion. Thus, we hypothesized now, that reduced or lack of hepatic arterial perfusion aggravates the primary damage and decelerates the recovery process, but does not influence the formation of vascular sinusoidal canals.

Materials and methods: Male Lew rats were subjected to RMHV-L+/-additional dearterialization and additional arterialized versus non-arterialized syngeneic liver transplantation. Experimental readout included liver damage (extent of necrosis (macroscopy, morphometry), liver enzymes, histology), hepatic microcirculation (OPS: sinusoidal diameter, VSC), liver regeneration (BrdU-LI) and vascular remodeling (Laminin, vW).

Results: "Ligation only" caused confluent necrosis interspersed with viable portal islands in the OZ. Within 1week, VSC with visible blood flow and normal sinusoidal structure developed in the border zone. Additional dearterialization caused full necrosis without any viable portal islands in OZ. On POD28 only single large draining VSC without any neighbouring normal hepatic parenchymal structure were found. Additional transplantation injury further aggravated the extent of damage and slowed down the recovery process.

Conclusion: VSC formed under all experimental conditions tested ensuring the drainage of the obstructed territory. Hepatic arterial perfusion was essential for spontaneous parenchymal recovery. Reduction of portal hypertension after PH should improve hepatic arterial perfusion, which is tested in the subsequent ongoing study.