Liver microvascular architecture: an insight into the pathophysiology of portal hypertension

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 retractability 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.