Cuddy B G, Loegering D J, Blumenstock F A
Proc Soc Exp Biol Med. 1984 Sep;176(4):443-51. doi: 10.3181/00379727-176-41896.
Previous studies have implicated a role for impaired hepatic macrophage blood clearance function in the increased susceptibility to infection caused by experimental thermal injury. The present study evaluated in vivo hepatic macrophage complement receptor clearance function as a possible factor contributing to impaired hepatic clearance after thermal injury. Rat erythrocytes treated with anti-erythrocyte serum (EA) were used as the test particle in rats. EA were rapidly removed from the circulation primarily by the liver and hepatic uptake of EA was greatly depressed in animals rendered C3 deficient by treatment with cobra venom factor. Thermal injury caused a large depression in the hepatic uptake of EA. It was shown that the depression in the binding of EA to hepatic macrophages was not due to decreased hepatic blood flow, decreased serum complement levels, or increased fluid phase C3b. Also, the depression of the hepatic uptake of EA incubated with serum prior to injection (EAC) was not different from that of EA after thermal injury. On this basis it was concluded that the impairment in binding of EA to the macrophages was at the cellular level and represented a depression in complement receptor clearance function. Additional studies showed that the injection of erythrocyte stroma, as a model of intravascular hemolysis, also depressed in vivo hepatic macrophage complement receptor clearance function. This latter finding suggests that the intravascular hemolysis caused by thermal injury may contribute to the depression of macrophage receptor function. The depression of hepatic macrophage complement receptor clearance function may contribute to the impaired bacterial clearance and increased susceptibility to infection following experimental thermal injury.
先前的研究表明，肝脏巨噬细胞血液清除功能受损在实验性热损伤所致感染易感性增加中起作用。本研究评估了体内肝脏巨噬细胞补体受体清除功能，作为热损伤后肝脏清除功能受损的一个可能因素。用抗红细胞血清（EA）处理的大鼠红细胞用作大鼠的测试颗粒。EA主要通过肝脏迅速从循环中清除，在用眼镜蛇毒因子处理使C3缺乏的动物中，肝脏对EA的摄取大大降低。热损伤导致肝脏对EA的摄取大幅降低。结果表明，EA与肝脏巨噬细胞结合的降低不是由于肝血流量减少、血清补体水平降低或液相C3b增加。此外，注射前与血清孵育的EA（EAC）的肝脏摄取降低与热损伤后EA的降低没有差异。在此基础上得出结论，EA与巨噬细胞结合的受损是在细胞水平，代表补体受体清除功能降低。进一步的研究表明，作为血管内溶血模型的红细胞基质注射也降低了体内肝脏巨噬细胞补体受体清除功能。后一发现表明，热损伤引起的血管内溶血可能导致巨噬细胞受体功能降低。肝脏巨噬细胞补体受体清除功能降低可能导致实验性热损伤后细菌清除受损和感染易感性增加。
