Hepatic neovascularization after partial portal vein ligation: novel mechanism of chronic regulation of blood flow

The present study was undertaken to investigate hepatic microcirculatory re sponse following partial portal vein ligation (PPVL) in rats. Portal pressu re was markedly increased 2-6 wk after PPVL, but no significant reduction i n sinusoidal perfusion and hepatocellular injury were detected. However, ma rked neovascularization was observed in PPVL rats using intravital microsco py and scanning electron microscopy (SEM). Extremely high red blood cell ve locity (2,000-4,900 mum/s) was seen in these vessels. Injection of fluoresc ein sodium via the carotid artery revealed that the neovessels originated f rom the hepatic arterial vasculature. This was further confirmed by clampin g the common hepatic artery and phenylephrine injection from the carotid ar tery. These vessels maintained sufficient flow after massive sinusoidal shu tdown elicited by the portal infusion of endothelin receptor B agonist IRL- 1620. SEM also showed extensive neovascularization at the hilum. Additional ly, clamping the portal vein decreased sinusoidal perfusion only by 9.5% in PPVL, whereas a 71.2% decrease was observed in sham. These results strongl y suggest that the liver maintains its microcirculatory flow by vascular re modeling from the hepatic arterial vasculature following PPVL.