CL of PMNL was decreased in the early stage of hemorrhagic shock in the rat if evaluated from whole blood. When standardized PMNL were incubated with plasma of different shock states the same serum--mediated depression was observed. In all stages killing activity of PMNL per se from arterial blood (after passage of pulmonary endothelium) was nearly unchanged if measured in standardized pool plasma. Furthermore in the prefinal stage of uncompensated shock highly activated PMNL were obtained. These results support the hypothesis that plasmatic--cellular interactions play an important role in depression of killing activity of PMNL already in early hemorrhagic shock. Actual concepts mention protein cleavage products, fluid phase C3b and prostaglandins as potential mediators of this serum--mediated suppression.