Transsinusoidal fluid dynamics in canine liver during venous hypertension.

Abstract

SUMMARY We studied arterial pressure, portal pressure, inferior vena caval pressure, hepatic interstitial pressure (implanted capsule technique), prenodal lymph flow, and the protein concentration in plasma and lymph in the anesthetized dog under normal conditions and during graded venous hypertension resulting from inferior vena caval occlusion. Under control conditions, portal, interstitial, and inferior vena caval pressures were 7.0, 5.8, and 2.0 mm Hg, respectively, and the lymph-plasma protein concentration ratio was 0.95. During acute venous hypertension, 64% of the inferior vena caval pressure increase was transmitted to the hepatic interstitium, and lymph flow increased 63% for every 1 mm Hg increment in interstitial pressure. The lymph-plasma protein concentration ratio did not change significantly during venous hypertension, indicating that: (1) the reflection coefficient of the sinusoidal wall for the major plasma proteins is close to zero, and (2) protein transport across the microvascular wall is due mainly to bulk flow. Using portal, interstitial, and inferior vena caval pressures as limits for possible values of sinusoidal pressure, our data suggest that (1) control sinusoidal pressure was between 5.8 and 7.0 mm Hg, and (2) approximately 90% of the increase in inferior vena caval pressure was transmitted to the sinusoids. The results indicate that changes in interstitial pressure, lymph flow, and surface transudation rate are major compensatory mechanisms operating in the liver to limit interstitial engorgement during venous hypertension. CireRea 45:317-323, 1979 THE LIVER, with its extensive vasculature and leaky sinusoids, plays a central role in the control of blood volume and cardiovascular fluid dynamics. More specifically, the high compliance of the hepatic vessels allows the liver to serve as a blood reservoir for maintenance of adequate cardiovascular filling during hemorrhage (Lautt and Greenway, 1976). In addition, in certain clinical conditions such as congestive heart failure, the free communication of the liver interstitium with the potential space of the peritoneal cavity provides a convenient route for spillage of excess plasma out of the circulation via the hepatic sinusoids (Greenway and Lautt, 1970). In general, transsinusoidal fluid flux should be governed by the same hydrostatic and oncotic forces that determine fluid movement across the capillary wall of other tissues (Starling, 1896). Unfortunately, the magnitude of each sinusoidal and