Intravascular hemolysis and RES phagocytic and host defense functions.
Depression of the reticuloendothelial system (RES) is thought to contribute to the pathogenesis of circulatory shock and to the increased susceptibility to infection following injury. An important aspect of the data supporting this concept is the observation that the phagocytosis of foreign particulates induces a period of RES depression and increased susceptibility to shock and infection. Since the RES normally removes altered autologous material from the circulation, the possibility exists that the phagocytosis of autologous material may induce an RES depression in the same way as the experimental RES uptake of foreign particulates. Thermal injury causes hemolysis with the generation of disrupted and damaged red blood cells (RBC), and this form of injury is followed by marked depression of host defense. Recent studies have demonstrated that simulation of intravascular hemolysis by the injection of hemolyzed blood causes a depression of RES phagocytic function. This effect was due to the particulate stroma component of the hemolyzed blood. RBC stroma was found to be rapidly removed from the circulation by the phagocytic cells of the liver. The RES depression induced by hemolyzed blood or RBC stroma was associated with an increased susceptibility to hemorrhagic shock, endotoxin shock, and septic shock. Additionally, the dose of hemolyzed blood required to depress the RES represented about 2.8% of the blood volume and thermal injury was found to cause acute intravascular lysis of 3.1% of the RBC mass, indicating that sufficient RBC debris can be generated to depress the RES by thermal injury. Thus, the generation and subsequent phagocytosis of altered autologous material, particularly RBC, may play an important role in the depression of RES phagocytic and host-defense functions following thermal injury.
D000818:Animals; D002056:Burns / Q000503:physiopathology; D004285:Dogs; D004912:Erythrocytes / Q000502:physiology; D006461:Hemolysis; D012157:Mononuclear Phagocyte System / Q000503:physiopathology*; D010587:Phagocytosis; D051381:Rats; D012769:Shock / Q000209:etiology* / Q000503:physiopathology