Local Factors in the Pathogenesis and Course of Experimental Ascites

¹ From the Department of Physiology, Medical College of Georgia, Augusta, Georgia

The evolution of the ascites of hepatic venous congestion was studied in dogs, following constriction of the thoracic inferior vena cava. Ascites developed in accordance with measurable changes in the transmembrane forces responsible for the net flux of fluid between extracellular fluid compartments. On the other hand, the volume of ascitic fluid could be modified with infinitesimal changes in transcompartmental pressure gradient. Although increased venous pressure appears to be the initial factor in the formation of the ascites of hepatic venous congestion, a most important factor is the permeability of the liver capsule which is stressed by elevated transmural pressure. Transudation of liver tissue fluid results. In this type of ascites, indirect calculations of the effective portal or mesenteric capillary pressure from the colloidal osmotic pressure difference between blood plasma and ascitic fluid, in accordance with the Starling equilibrium equation, are quite erroneous. Paradoxically, the ascites of venous congestion of the liver may disappear spontaneously, in spite of no reduction in the degree of hepatic venous hypertension, because of fibrosis of the liver capsule which reduces its permeability to water crystalloid and colloid.