The dynamics of "reticuloendothelial blockade" were studied in living rabbits and isolated, perfused rabbit livers utilizing gelatin as a blockading agent and Au198 stabilized in gelatin as a tracer.
Employing the above experimental model, the following observations were made. (a) RES blockade was specific and dependent on the surface properties of the particle under study. (b) RES blockade was not caused by saturation of hepatic removal mechanisms. (c) RES blockade was not caused by depletion of demonstrable serum opsonins. (d) RES blockade appeared to correlate with high circulating levels of the blockading agent, per se.
Thus, under the conditions employed, the term "reticuloendothelial blockade" was a misnomer. Although specificity of liver macrophage-particle interaction was evident and deserves further study, the data suggest that blockade as usually studied is a laboratory phenomenon induced by the continuing circulation of the blockading agent.