Effect of extravascular hemolysis on the RES depression following thermal injury.
This study was carried out to determine if the reticuloendothelial system (RES) uptake of damaged red blood cells (RBC) following thermal injury is sufficient to depress hepatic and splenic clearance function or to increase susceptibility to endotoxin shock. This was approached by determining the extent of the RES uptake of intact RBC (extravascular hemolysis) following thermal injury in rats, and by determining the effect on RES function of a similar degree of extravascular hemolysis induced in uninjured animals by the injection of heat damaged RBC. The RES uptake of three doses of heated RBC was characterized and the second largest dose caused a degree of extravascular hemolysis which was comparable to that associated with thermal injury. This latter dose of heated RBC depressed splenic clearance function but did not depress hepatic clearance function as determined using the smallest dose of heated RBC or formalinized sheep red blood cells at the test particles. Susceptibility to endotoxin shock was increased following the injection of the dose of heated RBC which stimulated the degree of extravascular hemolysis associated with thermal injury. Thus, the extravascular hemolysis associated with thermal injury is sufficient to depress splenic clearance function but not hepatic clearance function, and may contribute to the increased susceptibility to endotoxin shock following thermal injury. These findings further support the hypothesis that the hemolysis induced by thermal injury contributes to the depression of host defense associated with this form of injury.
D000818:Animals; D002056:Burns / Q000276:immunology*; D004912:Erythrocytes / Q000276:immunology; D006461:Hemolysis; D008099:Liver / Q000276:immunology; D008297:Male; D012157:Mononuclear Phagocyte System / Q000276:immunology*; D051381:Rats; D011919:Rats, Inbred Strains; D012772:Shock, Septic / Q000276:immunology; D013154:Spleen / Q000276:immunology