ABSTRACT
Structural adaptations in the liver to constantly receive and release a large volume
of circulating blood at low pressure are present at many levels; alteration of these
structures can modify flow and perturb pressure gradients. Liver growth multiplies
the lobule number by a factor of 4-5 after birth. Lobule configuration conforms with
observations in space division, each unit being bordered by planes; curvature will
impede expansibility and retractabil-ity among units. Lobular organization with hepatocytic
plates and sinusoids, being radial centrally and reticular peripherally, maximizes
its reversible distensibility. Resistance sites in the portal, sinusoidal, and hepatic
system are subject to species variations; real portal sphincters are photographed
in the frog. Small venules are demonstrably resistive. In endothelin-1-induced rat
portal hypertension, the distal segment of preterminal portal venules constricts most
intensely, whereas the terminal portal venules and sinusoids are flaccid. Their pericytes
and arachnocytes (stellate cells, Ito cells, retinol-storing cells), respectively,
possess no effective contractile machinery. In the dog, the initial sublobular veins
react with venoconstriction to many stimulations. Well-developed musculature in hepatic
veins, as in man and pig, can regulate flow by junctional constriction. These histoarchitectonics
provide hepatic hemodynamics with high capacitance and high compliance properties.
The hepatic artery supplies oxygenated blood to five stromal compartments: peribiliary
vascular plexus, portal tract interstitium, portal vein vasa vasorum, hepatic capsule,
and central-sublobular-hepatic vein vasa vasorum. Its role as the nutrient vessel
to the veins is established, but what influence it may have in the pathophysiology
of portal hypertension awaits clarification.
KEY WORDS
liver lobule - portal vein - sinusoid - hepatic vein - hepatic artery
