Spontaneous portosystemic shunting as a consequence of liver cirrhosis leads to a hypercirculatory syndrome as well as to changes in blood distribution of different organs. These circulatory alterations, characterized by increased cardiac output, intrapulmonary venous admixture, decreased peripheral vascular resistance and increased systolic ejection rate are also found in rats with portocaval anastomosis (PCA), a well established experimental model (Herz et al. 1972, Liehr et al. 1976). In previous studies we could demonstrate that also distribution of PO2 in skeletal muscle of these animals is influenced by a PCA. Under normoxic conditions mean muscular PO2 decreases after an initial rise, and reaches about 200 days after operation the level of control animals with persisting signs of maldistribution (Heinrich et al. 1984, 1984). The following experiments were done to evaluate whether late after PCA regulation of muscle PO2 is altered under hypoxic, hyperoxic and hypercapnic conditions.
