The effect of various hepatic vein pressures on hepatic hemodynamics, on fluid shifts within the liver, and on certain indices of liver function were studied in the isolated rat liver preparation. In general, venous pressures are scarcely perceived by the hepatic parenchyma unless they exceed the hydrostatic pressures acting at the liver surface, more particularly at the hilum of the liver. Venous pressures exceeding this value appear to distend the liver vasculature so that it acts like a system of rigid conduits; there is great expansion of the sodium space and of the colloid distribution spaces, and some evidence of partial sequestration of blood in the congested liver. All these changes impair oxygen supply to the tissue. To a lesser extent they interfere with the transfer of other substances from blood to parenchyma, and place considerable stress upon the mechanical framework of the liver. The resulting strain in turn tends to limit the extent of intrahepatic changes in passive congestion, and possibly the rate of fluid leakage from blood via parenchyma to transudate at the liver surface.
A method has been described which allows the insertion of microneedles into minute blood vessels of the transilluminated rat liver. Using dye injections under controlled pressures and direct observation, blood pressures in the terminal portal venules as well as in the central veins of this preparation have been determined and have been compared with simultaneous pressure measurements in the mesenteric veins and in the vena cava at the level of entry of the hepatic veins. The results indicate an unexpectedly large pressure drop in the portal venous tree (from 13 cm H2O in the portal vein to approximately 6 cm in the portal venules), a significant pressure drop between portal venules and central veins (from 6 to 2.5 cm H2O), and a paradoxical mean pressure relation between central vein and vena cava. Discussion of these results has been presented in terms of methodological problems, the implication of the results for the control of blood flow distribution in the liver, and the intermittency of hepatic vein flow in the rat.
P32-labeled chromic phosphate colloid disappears from the circulation of the isolated rat liver preparation according to a single exponential term of time. A small nonextracted contaminant, less than 3% of the total activity is also detected. At comparable blood flow rates the colloid is extracted about as completely by the isolated liver preparation as by the liver in situ in the intact animal. The efficiency with which chromic phosphate colloid is removed from perfusate passing through the isolated rat liver decreases with increasing perfusion rate. If whole blood is used as a perfusate, the efficiency of colloid extraction is almost twice as high as it is if rat blood plasma is employed, even if adequate oxygenation of the tissue is assured by high oxygen partial pressures in the latter series. A theoretical treatment of these results is given in terms of first order reaction kinetics. Agreement of experimental results with this theory at perfusion rates greater than 2 cc/gm/min. indicates that the rate of chromic phosphate colloid extraction is a function of plasma concentration of the colloid, and that the extraction efficiency for a given perfusate varies as a function of the mean transit time of perfusate through the liver. Deviations from the predictions of the theory occur at low perfusion rates, and are discussed in the light of the above concepts. A decrease of the ratio of transit time to perfusion rate under these conditions suggests a decrease in the number of channels open to blood flow at low perfusion pressures.
Functional changes in the regenerating hepatic tissue as indicated by CrPO4 colloid extraction and bile secretion by the isolated rat liver preparation were studied. Following partial hepatectomy, the liver weight/body weight ratio of the operated rats is significantly lower than the nonoperated controls. This is attributed to only a 80–85% restoration of the residual hepatic tissue. A transient increase in bile secretion/ unit weight of liver by 50% above the preoperative level occurs within 48 hours after partial resection. The uptake of radioactive chromic phosphate colloid indicates an increase in Kupffer cell activity (phagocytic functions) to values 200% above control within 48 hours. This function, however, is sustained and remains elevated for at least 90–100 days postoperatively. Histological evidence indicates that the increased Kupffer cell activity is probably due to an increase in cell population of phagocytic cells. Theoretical considerations for these changes in specific function of regenerating hepatic tissue and their relation to normal resting liver are discussed.
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