THERMAL INJURY, COMPLEMENT, AND LEUKOCYTE DYSFUNCTION

现在有明确的证据表明补体激活和白细胞功能障碍 在急性热损伤期间。 拟议的研究将调查以下方面的证据： 大鼠急性烫伤时补体激活的研究 补体成分 将测量溶血活性以及C3代谢的变化。 系统动脉血压和血气的变化将 在热损伤期间监测与体内补体激活相关的情况， 补体激活产物、中性粒细胞和 评估前列腺素生物合成途径。 肺内隔离症 中性粒细胞和血小板在热损伤期间将被测量和相关 体内补体激活。 将监测白细胞是否获得 急性热损伤时的白细胞定向功能障碍，特别是 去活化 趋化因子（chemotactic factor） 灭活剂、细胞定向抑制剂和白细胞分裂增强因子）将被 在急性热损伤期间测量。 最后，我们将尝试确定是否 以及热损伤组织以何种方式激活补体系统， 直接将C3或C5片段化成具有生物活性的 产品. 这项全面的研究应界定补语的作用 系统在热损伤过程中发生的病理生理变化， 白细胞定向缺陷的性质。

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.