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

Structural adaptations in the liver to constantly receive and release a lar ge volume of circulating blood at low pressure are present at many levels; alteration of these structures can modify flow and perturb pressure gradien ts. Liver growth multiplies the lobule number by a factor of 4-5 after birt h. Lobule configuration conforms with observations in space division, each unit being bordered by planes; curvature will impede expansibility and retr actability among units. Lobular organization with hepatocytic plates and si nusoids, being radial centrally and reticular peripherally, maximizes its r eversible distensibility. Resistance sites in the portal, sinusoidal, and h epatic system are subject to species variations; real portal sphincters are photographed in the frog. Small venules are demonstrably resistive. In end othelin-1-induced rat portal hypertension, the distal segment of pretermina l portal venules constricts most intensely, whereas the terminal portal ven ules and sinusoids are flaccid. Their pericytes and arachnocytes (stellate cells, Ito cells, retinol-storing cells), respectively, possess no effectiv e contractile machinery. In the dog, the initial sublobular veins react wit h venoconstriction to many stimulations. Well-developed musculature in hepa tic veins, as in man and pig, can regulate flow by junctional constriction. These histoarchitectonics provide hepatic hemodynamics with high capacitan ce and high compliance properties. The hepatic artery supplies oxygenated b lood to five stromal compartments; peribiliary vascular plexus portal tract interstitium portal vein vasa vasorum, hepatic capsule, and cental-sublobu lar-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 p ortal hypertension awaits clarification.