Our recent studies of skin thermal injury in rats have demonstrated the onset of systemic activation of complement, acquisition of phagocytic cell defects and development of secondary lung injury. The pulmonary complication has been related to intravascular activation of neutrophils, entrapment of leukoaggregates in lungs and the development of pulmonary vascular endothelial injury due to oxygen radical (hydroxyl radical) formation by leukocytes. We now plan to examine both local effects of thermal injury as well as some of the systemic complications (phagocytic cell defects and intravascular hemolysis) arising from localized thermal injury of skin. The proposed studies will focus on mediator systems responsible for the local inflammatory response to thermal injury, the ability of thermally injured parenchymal and mesenchymal cells to activate the complement system, mediators responsible for the acquired defects of phagocytic cells following thermal injury, and the pursuit of preliminary evidence suggesting that intravascular hemolysis associated with thermal injury is probably the combined result of intravascular activation of complement as well as oxygen radical generation by blood neutrophils. The development of flow cytometric techniques to analyze in a quantitative manner unfractionated blood leukocytes from small volumes (0.1 ml) of whole rat blood will greatly facilitate these studies.
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