[The behavior of albumin in acute and chronic liver diseases. I. The behavior of albumin during the development of rat thioacetamide cirrhosis].

The behaviour of albumin during the development of chronic progressing liver damages was investigated on the model of the thioacetamide cirrhosis in Wistar-rats. Simultaneous estimations of the albumin concentrations in extractable liver protein and in the serum as well as accompanying measurements of the total protein and of the transaminases SGOT and SGPT in the serum allow a complex judgment. The albumin concentration in the liver significantly decreased after 4 and 8 weeks and reached highly normal values in fully developed cirrhosis. In each case the serum level changed in the same sense, but less expressed. The total protein in liver and serum showed an analogous course of the curve, whereas the albumin-total protein-quotient in the liver remained unchangedly low. The relative proportion of albumin in the serum did not show a diminution in every phase. The simultaneous decrease of albumin and total protein are explained as an expression of an inhibition of the synthesis due to destruction of protein-synthesizing subcellular structures. The normalisation of the serum levels and of the highly normal albumin contents despite the developed cirrhosis become understandable by the loss of efficiency of the foreign substance thioacetamide in consequence of structural and biochemical adaptation. The thioacetamide cirrhosis of the rat in the investigated phase despite the microscopically provable so-called degenerative parenchymal damages is accompained by parameters of the increased protein metabolism. The relative serum albumin content apparantly in the first place undergoes the oncotic pressure regulation and is not suited as the measure of a hepatocellular lesion. From the diagnostic point of view the reduction of the albumin concentrations seems to be of importance in the developmental phase to cirrhosis.