There is now clear evidence of complement activation and leukocyte dysfunction during acute thermal injury. The proposed studies will investigate evidence for complement activation during acute thermal injury in rats. Complement component hemolytic activities will be measured as well as changes in C3 metabolism. Changes in systematic arterial blood pressure and in blood gases will be monitored in relation to in vivo complement activation during thermal injury and the pathophysiological roles of complement activation products, neutrophils and the prostaglandin biosynthetic pathways assessed. Intrapulmonary sequestration of neutrophils and platelets during thermal injury will be measured and related to in vivo complement activation. Leukocytes will be monitored for acquired leukotactic dysfunction during acute thermal injury, with special reference to deactivation. Changes in leukotactic regulatory factors (chemotactic factor inactivator, cell directed inhibitor and leukokinesis enhancing factor) will be measured during acute thermal injury. Finally, we will try to determine whether and in what manner thermally injured tissue activates the complement system or directly brings about fragmentation of C3 or C5 into biologically active products. This comprehensive study should define the role of the complement system in the pathophysiological changes developing during thermal injury and the nature of the leukotactic defects.
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