The Role of C5 in Septic Lung Injury
The Role of C5 in Septic Lung Injury
复制标题
C5 在脓毒性肺损伤中的作用
DOI：
10.1097/00000658-198512000-00018
复制
发表时间：
1985
影响因子：
9
通讯作者：
T. K. Das Gupta
中科院分区：
文献类型：
--
作者：
L. Olson;G. Moss;O. Baukus;T. K. Das Gupta
One proposed mechanism for the pathogenesis of lung injury in septic animals is the stimulation by C5a of granulocytes to produce and release toxic oxygen radicals that damage cellular membranes in pulmonary capillaries. The authors have investigated the possible role of C5 in septic lung injury, utilizing C5-sufficient and C5-deficient twin mice strains. In this lethal sepsis model, mean survival time is increased in C5-deficient mice in comparison to the survival of their C5-sufficient twins. Morphometric results demonstrate a significant increase in intracapillary granulocrit and air-blood barrier thickness 24 hours after cecal ligation and puncture in C5-sufficient septic mice. Similarly, mean arterial pO2 is significantly decreased in the C5-sufficient animals. Intracapillary granulocrit, air-blood barrier thickness, and arterial pO2 are normal in the septic C5-deficient twins of these animals. These data support the hypothesis that C5 is involved in the pathogenesis of septic lung injury.
