HEPATIC-ARTERY AND PORTAL-VEIN VASCULARIZATION OF NORMAL AND CIRRHOTIC RAT-LIVER

The hepatic artery and portal vein vascularization of seven normal and seven cirrhotic rats was evaluated by means of the multiple-indicator dilution technique using the how-limited model analysis. Injected 15-mu m microspheres were all trapped by the liver in normal and cirrhotic rats after portal vein and hepatic artery injections, ruling out the presence of intrahepatic shunts larger than 15 mu m. The albumin curve was linearly displaced relative to the red blood cell curve in both groups of rats, indicating that albumin distribution remained compatible with the flow-limited distribution model. Albumin extravascular space was similar when measured following both routes of injection. Sucrose outflow profile was also compatible with the how-limited model after portal vein injection in normal rats, but not in severely cirrhotic rats. In contrast, after hepatic artery injection in both normal and cirrhotic rats the sucrose curve was not linearly displaced compared with that of red blood cells; its curve peak was less delayed than its downslope. This finding indicates that, after hepatic artery injection, sucrose distribution was not compatible with the how-limited model; moreover, its extravascular space was much larger than that after portal vein injection, particularly in cirrhotic rats. This phenomenon is best explained by the peribiliary capillary plexus, lying between terminal arteries and sinusoids, a plexus enlarged in cirrhotic livers. Finally, sinusoidal volume was apparently much larger after hepatic arterial injection compared with that after portal venous injection. This occurrence may well result from an unshared arterial sinusoidal bed or the peribiliary capillary plexus.