Drutz D J, Koenig M G, Rogers D E
J Exp Med. 1967 Dec 1;126(6):1087-98. doi: 10.1084/jem.126.6.1087.
The mechanism of the reticuloendothelial "blockade" which followed injection of large quantities of chromic phosphate without exogenous stabilizing material was investigated in Wistar rats. The RE blockade observed for several hours after induction appeared related to the continuing circulation of the chromic phosphate-blockading dose, and a reduction in the size of the particles used enhanced blockade. RE blockade appeared to be particles specific and was not related to a generalized depression of RE-phagocytic cell function. Studies in isolated perfused rat livers appeared to eliminate saturation of particle-specific macrophage clones as a likely explanation of blockade, and blockade could not be explained on the basis of depletion of serum opsonins. In the system employed, it is postulated that blockade occurs when large numbers of circulating particles saturate specific macrophage cell membrane-binding sites rather than from physical stuffing of RE-phagocytic cells.
在Wistar大鼠中研究了在无外源性稳定物质的情况下注射大量磷酸铬后发生的网状内皮系统“阻断”机制。诱导后数小时观察到的网状内皮系统阻断似乎与磷酸铬阻断剂量的持续循环有关，并且所用颗粒尺寸的减小增强了阻断作用。网状内皮系统阻断似乎具有颗粒特异性，与网状内皮吞噬细胞功能的普遍抑制无关。对离体灌注大鼠肝脏的研究似乎排除了颗粒特异性巨噬细胞克隆饱和作为阻断可能解释的可能性，并且不能基于血清调理素的消耗来解释阻断。在所采用的系统中，推测当大量循环颗粒使特异性巨噬细胞膜结合位点饱和时会发生阻断，而不是由于网状内皮吞噬细胞的物理填充。
