α-2-Glycoprotein Opsonic Deficiency after Trauma 1

Abstract

Summary

The present study evaluated the relative humoral and cellular contribution to post-traumatic reticuloendothelial phagocytic depression in an in vitro phago-cytic system. It was found that there is a severe depression of the humoral α-2-glyco-protein support of phagocytosis but no hepatic RES cellular deficit after severe trauma. It was additionally determined that transfer of plasma from traumatized animals into normal recipient animals and into the in vitro phagocytic system does not result in phagocytic depression, nor do hypoxia and acidosis impair phagocytosis in vitro. It is concluded that the post-traumatic reticuloendothelial phagocytic depression is primarily mediated by diminished humoral support rather than by cellular dysfunction and that the humoral deficit is a lack of opsonic activity rather than a phagocytic-depressant substance or hypoxic or acidotic conditions.