Anti‐Ascites Adaptation of Liver to Sinusoidal Hypertension

Abstract

The hepatic capsule is highly permeable to water and proteins. Increases in sinusoidal pressure as low as 1 mmHg have been reported to significantly elevate transudation across the capsule into the peritoneal cavity under normal conditions. However, despite the fact that hepatic sinusoidal and interstitial fluid pressures are significantly elevated with cirrhosis, transudation across the capsule is minimal and there is a lack of ascites. Because hepatic lymphatic vessels and thoracic ducts are enlarged and lymph flows are several times higher than normal levels, lack of ascites in compensated cirrhosis has been commonly ascribed to enhanced hepatic lymph flow. However, changes in capsular properties have yet to be investigated thoroughly. Therefore, the purpose of this study was to evaluate our hypothesis that sustained sinusoidal hypertension leads to decrease in capsular permeability and transudation rate. Capsular hydraulic conductance, reflection coefficient, transudation rate and hepatic lymph flow rate were evaluated following short‐term (2–3 weeks; StSH) and long term (5–6 weeks; LtSH) exposure to sinusoidal hypertension. Although hepatic capsular transudation and lymph flow rates were elevated in both groups, capsular hydraulic conductance and the transudation rate were lower and the reflection coefficient was higher in LtSH. Furthermore, comparison of hepatic interstitial fluid pressure‐lymph flow and hepatic interstitial fluid pressure‐transudation relationships revealed decreased sensitivity of capsular transudation to changes in hepatic interstitial fluid pressure in LtSH. Taken together, these findings suggest that adaptation of hepatic capsule precedes the enlargement of the hepatic lymphatic vessels and may primarily be responsible for the lack of ascites in compensated cirrhosis.