A biphasic model for sinusoidal liver perfusion remodeling after outflow obstruction.
Liver resection can lead to focal outflow obstruction due to transection of hepatic veins. Outflow obstruction may cause additional damage to the small remnant liver. Drainage of the obstructed territories is reestablished via dilatation of sinusoids. Subsequently, sinusoidal canals are formed draining the blood from the obstructed territory to the neighboring unobstructed territories. We raised the phenomenological hypothesis that the blood pressure gradient is the main driving force for the formation of sinusoidal vascular canals. We generated a biphasic mechanical model to describe this vascular remodeling process in relation to the variable pressure gradient. Therefore, we introduced a transverse isotropic permeability relation as well as an evolutional optimization rule to describe the relationship between pressure gradient and the direction of the sinusoidal blood flow in the fluid phase. As a next step, we developed a framework for the calculation concept including the representation of the governing weak formulations. Then, we examined a representative numerical example with simulation of the blood flow under both conditions, the physiological situation as well as after outflow obstruction. Doing so, we were able to reproduce numerically the experimentally observed process of reestablishing hepatic venous drainage via redirection of blood flow and formation of new vascular structures in respect to the fluid flow. The calculated results support the hypothesis that the reorientation of blood flow mainly depends on the pressure gradient. Further investigations are needed to determine the micromechanical influences on the reorientation of the sinusoids.
Ricken
Tim
T
University of Duisburg-Essen, Essen, Germany. tim.ricken@uni-due.de
Dahmen
Uta
U
Dirsch
Olaf
O
D000818:Animals; D006504:Hepatic Veno-Occlusive Disease / Q000503:physiopathology*; D006801:Humans; D008102:Liver Circulation / Q000502:physiology*; D023421:Models, Animal; D008954:Models, Biological; D010477:Perfusion; D051381:Rats