Hepatic arterial microvasculature

The hepatic arterial microvasculature comprises the terminal branches of the hepatic artery (terminal arterioles) and their communications that feed the hepatic sinusoids, notably the peribiliary plexus, terminal arteriosinus twigs, vasa vasorum on the portal vein, and direct arterioportal anastomoses. In normal liver, oxygenated arterial blood mixes with portal venous blood within the sinusoidal network of the hepatic acinus/lobule, establishing zonal gradients in oxygen and metabolism. Arterial flow participates in the hepatic arterial buffer response and shear stress–dependent endothelial nitric oxide signaling that influences hepatocyte volume and regeneration pathways. These microvascular pathways are clinically pivotal in interventional oncology: transarterial therapies and hepatic arterial infusion exploit the predominant arterial supply of liver tumors and the distribution characteristics of embolic/drug carriers within the microcirculation. In HCC, tumor biology and outcomes are linked to microvascular features such as microvascular invasion, and anti-angiogenic agents target signaling pathways governing arterialized tumor vasculature, not the normal microvasculature itself.

Other names

hepatic arterial microcirculationhepatic arteriolar networkperibiliary arterial plexus and arterioportal communications (components within the hepatic microcirculation)

Regional delivery/embolization: catheter-based hepatic arterial infusion and embolization leverage arterial microvascular supply to concentrate drugs or occlude tumor feeders; iodized oil can pass via peribiliary plexus into portal vein and through sinusoids. Systemic anti-angiogenesis in HCC: inhibition of VEGFR and other kinases reduces tumor arterial neovascularization (e.g., sorafenib multikinase inhibition; ramucumab targets VEGFR2 in AFP-high HCC).