Pipy B, de Maroussem D, Beraud M, Derache P
J Reticuloendothel Soc. 1983 Nov;34(5):395-412.
The simultaneous injection of carbaryl and colloidal carbon phagocytized by the reticuloendothelial cells results in competition between the two substances in favor of the carbon particles. Experiments with opsonized carbaryl suggest that the decrease in carbaryl blood clearance by the colloid is mediated by a depletion of serum opsonins. Following blockade, the liver carbaryl uptake was depressed in the control group (17%), while it was increased in the opsonized group (12%). With all preparations of carbaryl, opsonized or non-opsonized, colloidal carbon produced a slight and variable increase in carbaryl uptake by the spleen and lungs. These results indicate that, besides the uptake of carbaryl by the hepatocytes, other clearance sites must also be considered such as the Kupffer cells and other liver sinusoidal cells. Moreover our results show that intravenous administration of carbaryl induces a state of phagocytic depression as indicated by impaired intravascular phagocytosis and depressed hepatic uptake of the reticuloendothelial (RE)-test colloidal suspension. The results obtained from injection of opsonized colloidal particles during carbaryl-induced RE-depression, and the fact that carbaryl and carbon are both opsonized by the same serum factor, suggest that the mechanisms of RE-blockade involve selective hepatic and splenic macrophage failure and depletion of serum opsonins. According to our enzymatic investigation, this failure of the RE system to incorporate colloids during carbaryl--RE-blockade could be due to a defect in the activity of macrophage membrane-bound serine esterase.
同时注射西维因和被网状内皮细胞吞噬的胶体碳，会导致这两种物质之间产生竞争，使碳颗粒占优势。用调理素处理过的西维因进行的实验表明，胶体导致西维因血液清除率降低是由血清调理素耗竭介导的。阻断后，对照组肝脏对西维因的摄取降低了17%，而调理素处理组则增加了12%。对于所有西维因制剂，无论是否经过调理素处理，胶体碳都会使脾脏和肺对西维因的摄取略有增加且存在差异。这些结果表明，除了肝细胞对西维因的摄取外，还必须考虑其他清除部位，如库普弗细胞和其他肝窦细胞。此外，我们的结果表明，静脉注射西维因会诱导吞噬抑制状态，表现为血管内吞噬功能受损和网状内皮（RE）试验胶体悬浮液的肝脏摄取降低。在西维因诱导的RE抑制期间注射调理素处理过的胶体颗粒所获得的结果，以及西维因和碳都被同一血清因子调理的事实，表明RE阻断机制涉及选择性肝和脾巨噬细胞功能衰竭以及血清调理素耗竭。根据我们的酶学研究，在西维因-RE阻断期间RE系统无法摄取胶体可能是由于巨噬细胞膜结合丝氨酸酯酶活性缺陷所致。
