Involvement of the reticuloendothelial system (RES) in bacterial infection (1, 2), neoplastic disease (3,4), and immunological activity (5, 6) has been well documented. Such studies have emphasized the host defense role of the RES and the need to comprehend factors that induce changes in RE activity.Recent findings by Donovan (7) in humans, and Saba and Di Luzio (8) in animals have demonstrated that surgical manipulation will depress phagocytosis. Moreover, it has been speculated that the decreased resistance (9-10) and increased incidence of metastasis after surgical stress ( 11-1 5) may be due to depressed phagocytosis (8). Although previous findings have revealed the existence of phagocytic changes after surgery, the factors mediating this response have not been determined. Since phagocytic depression can occur as a result of a depletion of circulating plasma factors called opsonins (14, 15), R E depression after surgical stress may reflect a depression of opsonin activity.In the present study, the involvement of the opsonic system as a factor mediating RE depression after surgery was evaluated. In addition, the time course associated with surgically induced RE alteration as well as the colloid specificity of the response was evaluated.Experimental Methods. Male Holtzman rats (225-350 g) were maintained on Rockland Lab-Tek chow and tap water ad libitum Liver donors were anesthetized with ether and rapidly desanguinated prior to liver removal. The excised liver was chilled in cold isotonic saline prior to liver slice preparation with the use of a Stadie-Riggs tissue slicer