Lung injury secondary to chemotactic factor-induced leukocyte activation.
Lung injury secondary to chemotactic factor-induced leukocyte activation.
复制标题
趋化因子诱导的白细胞激活继发肺损伤。
DOI：
10.1007/978-3-0348-9352-7_24
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发表时间：
1983
期刊：
影响因子：
--
通讯作者：
Ward,PA
中科院分区：
文献类型：
--
作者：
Till,GO;Ward,PA
大鼠在热损伤或血管输注眼镜蛇毒因子后，血管内补体激活会导致急性肺损伤，这是通过形态学和肺血管通透性增加来测定的。急性肺损伤与循环中c5衍生的趋化活性的早期出现与中性粒细胞减少症的发生有关。肺损伤与补体和中性粒细胞的可用性密切相关，可以通过对动物进行全身治疗，结合使用超氧化物歧化酶和过氧化氢酶（有毒氧代谢物的特异性抑制剂）来预防。这些数据表明，血管内补体激活导致中性粒细胞的激活及其肺内毛细血管隔离，以及随后的急性肺损伤，这与c5a激活的血液中性粒细胞产生和释放氧源性自由基有关。
Intravascular complement activation in rats following thermal injury or vascular infusion of cobra venom factor results in acute lung injury as determined morphologically and measured by increases in lung vascular permeability. The acute lung injury is associated with the early appearance of C5-derived chemotactic activity in the circulation coincident with the development of neutropenia. The lung injury is closely linked to availability of complement and neutrophils and can be prevented by systemic treatment of animals with a combination of superoxide dismutase and catalase, specific inhibitors of toxic oxygen metabolites. These data suggest that intravascular complement activation leads to activation of neutrophils and their intrapulmonary capillary sequestration, and subsequent acute lung injury, which is associated with production and release of oxygen-derived free radicals by C5a-activated blood neutrophils.