Vascular Model of Liver Fibrosis

Abstract

Abstract The liver has a very peculiar blood circulatory system composed of two blood supply vascular trees (the hepatic artery and portal venous networks), microcirculation through small functional units called lobules, and a blood drainage vascular tree (the hepatic vein network). In the healthy liver, flow resistance at the microcirculation level is very low and the portal pressure is almost the same as the lobules pressure. On the other hand, vasculature changes due to fibrosis — located predominantly at the lobules level — lead to a marked increase in resistance to flow causing an increase in portal pressure (portal hypertension). Here, a rigid model of the entire liver vasculature is built, where hepatic networks are considered as tree-like fluidic networks and lobules as a porous medium. The model can provide the blood flow and pressure within their healthy physiological ranges at all points of the vasculature. To simulate liver fibrosis, the portal hypertension it causes is reproduced. The high portal pressure values reported for fibrotic patients are used to calculate the necessary lobules permeability resulting in these pressure values at the inlet of the lobules. The decrease in the permeability of the fibrotic lobules causes a redistribution of flow between the two blood supply networks. The alterations of microcirculation due to fibrosis are also analyzed: increases in blood flow through the non-fibrotic lobules and decreases in blood flow through the fibrotic ones are observed, relative to blood flow through the lobules in a healthy liver.