Plasma substitute induced impairment of the reticuloendothelial system function.

Currently used plasma substitutes are large colloids and are partly engulfed by reticuloendothelial (RE) cells. This study was designed to investigate the magnitude and duration of the possible RES dysfunction induced by plasma substitutes. The following substances were studied in both normal and burned (LD-10) CBA mice: allogen albumin 3%, and commercial preparations of dextran 40, dextran 70, hydroxyethyl starch, gelatin and PVP. Infusion volume was 20 ml/kg and i.v. infusion time 1 hour. Animals given allogen plasma served as controls. One, 3 and 6 hours after the i.v. injection of 51-Cr-rabbit RBC, we determined the disappearance rate, and uptake and distribution of the 51-Cr-RBC in the main RES organs (liver, spleen and lungs). In normal mice the disappearance rate was significantly decreased one and three hours post infusion, while it was decreased even after 6 hours in burned mice. Groups given albumin or plasma stayed close to non-infused animals. In order to clarify the physiologic significance of these findings we used another test substance known to be handled by the RES. Salmonella enteritidis endotoxin was tested with regard both to toxicity and rate of elimination. The toxicity, after i.p. injection, was significantly intensified both one and 3 hours post-infusion in normal mice. In burned mice toxicity became even more intense. The ability to eliminate 51-Cr-labelled endotoxin was significantly decreased following infusion in both normal and burned mice, one as well as three hours later. The in vitro liver phagocytosis was tested utilizing the liver slice technique. Standardized slices were incubated in Krebs-Ringer buffer together with 125-I-HSA aggregates as RES test substance with and without plasma from mice given plasma substitute infusions. Allogen plasma enhanced the phagocytic uptake (four times), while post-infusion plasma did not. It is concluded from these experiments, utilizing two different RES test substances in both normal and hypovolemic animals, that the plasma expanders tested do impair RES phagocytosis. The mechanism seems to be an interaction with phagocytosis-promoting plasma factors. Even though this impairment is temporary, it may jeopardize such important RES functions as elimination of microorganisms, toxins, cell debris and tumour cells, or spoil the afferent limb of the immune response to many antigens.