Transsinusoidal fluid dynamics in canine liver during venous hypertension.
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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: the reflection coefficient of the sinusoidal wall for the major plasma proteins is close to zero, and 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 control sinusoidal pressure was between 5.8 and 7.0 mm Hg, and 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.
