Bosch M A, Risco C, Martin-Municio A
Department of Biochemistry and Molecular Biology, Faculty of Chemistry, Universidad Complutense, Madrid, Spain.
Mol Cell Biochem. 1990 Mar 27;93(2):167-72. doi: 10.1007/BF00226188.
Alterations in pulmonary surfactant are partly responsible for the respiratory insufficiency seen under septic shock process. We have used an experimental model of LPS-induced shock in rats to examine the cells responsible for the pulmonary surfactant synthesis and its relationship to lung injury. (14C)Choline incorporation into phosphatidylcholine was significantly reduced in lung homogenates or type II cells obtained from LPS-treated animals. Addition of LPS in vitro fails to increase (14C)choline incorporation in type II cells obtained from LPS-treated animals. We suggest that this depression of pulmonary phosphatidylcholine synthesis may partly explain the occurrence of respiratory failure with septic shock.
肺表面活性物质的改变部分导致了脓毒性休克过程中出现的呼吸功能不全。我们使用脂多糖诱导的大鼠休克实验模型，来研究负责肺表面活性物质合成的细胞及其与肺损伤的关系。从脂多糖处理的动物获得的肺匀浆或II型细胞中，（14C）胆碱掺入磷脂酰胆碱的量显著减少。在体外添加脂多糖并不能增加从脂多糖处理的动物获得的II型细胞中（14C）胆碱的掺入量。我们认为，肺磷脂酰胆碱合成的这种抑制可能部分解释了脓毒性休克时呼吸衰竭的发生。
