Till G O, Beauchamp C, Menapace D, Tourtellotte W, Kunkel R, Johnson K J, Ward P A
J Trauma. 1983 Apr;23(4):269-77. doi: 10.1097/00005373-198304000-00001.
Acute thermal injury (70 degrees C, 30 sec) to rat skin results in progressive consumptive depletion of the complement system. Individual complement components (C3, C4, C6) each show reductions in hemolytic activity. Crossed immunoelectrophoresis analysis of serum from thermally injured rats reveals conversion of C3 compatible with activation of the complement system. During the first hour following thermal injury, C5a-related chemotactic activity appears in the serum and is temporally related to the development of neutropenia. Lung injury, as revealed by increases in lung permeability, develops progressively during a 6-hour period and parallels changes in complement levels. Morphologically, lung changes include leukoaggregates within pulmonary capillaries and the presence of intra-alveolar hemorrhage. Protection from lung injury following remote thermal injury to skin is afforded by depleting animals of complement or neutrophils, or by systemic treatment of animals with a combination of catalase and superoxide dismutase. Antihistamine drugs have no protective effect. These data suggest that acute thermal injury leads to systemic complement activation, neutrophil activation, and acute lung injury that is related to production of toxic oxygen products by activated blood neutrophils.
对大鼠皮肤进行急性热损伤（70摄氏度，30秒）会导致补体系统进行性消耗性耗竭。各个补体成分（C3、C4、C6）的溶血活性均降低。对热损伤大鼠血清进行交叉免疫电泳分析显示，C3发生转化，这与补体系统的激活相符。在热损伤后的第一个小时内，血清中出现与C5a相关的趋化活性，且与中性粒细胞减少的发生在时间上相关。如肺通透性增加所示的肺损伤在6小时内逐渐发展，并与补体水平的变化平行。形态学上，肺部变化包括肺毛细血管内的白细胞聚集和肺泡内出血。通过使动物的补体或中性粒细胞耗竭，或通过用过氧化氢酶和超氧化物歧化酶联合对动物进行全身治疗，可以防止皮肤远程热损伤后发生肺损伤。抗组胺药没有保护作用。这些数据表明，急性热损伤会导致全身补体激活、中性粒细胞激活以及与活化血液中性粒细胞产生有毒氧产物相关的急性肺损伤。
