von Wichert P, Wiegers U, Stephan W, Huck A, Eckert P, Riesner K
Res Exp Med (Berl). 1978 Jun 12;172(3):223-9. doi: 10.1007/BF01855832.
Pulmonary alterations after shock and sepsis, described clinically as shock lung or adult respiratory distress syndrome, are of great importance in intensive care. Pathogenetically an alteration of the surfactant system of the lung is often discussed. Since phospholipids are constituents of lung surfactants, phospholipid metabolism is investigated in experimental peritonitis in rats in our laboratory. 15 hours after inducing a peritonitis, the lung incorporates more oleic acid than that in animals of the reference group. 33 hours after inducing peritonitis, the capacity of the lung to incorporate choline and fatty acids is markedly reduced, histologically the lungs represent morphological equivalents of the so-called shock lung at this time. Therefore we conclude, that an alteration of phospholipid metabolism with a diminished and/or altered synthesis of lung surfactant plays, at least in part, an important role in the pathogenesis of respiratory distress in sepsis and peritonitis.
休克和脓毒症后的肺部改变，临床上称为休克肺或成人呼吸窘迫综合征，在重症监护中非常重要。在发病机制上，人们经常讨论肺表面活性剂系统的改变。由于磷脂是肺表面活性剂的组成成分，我们实验室在大鼠实验性腹膜炎中研究了磷脂代谢。诱发腹膜炎15小时后，肺摄取的油酸比对照组动物更多。诱发腹膜炎33小时后，肺摄取胆碱和脂肪酸的能力显著降低，此时在组织学上肺呈现出所谓休克肺的形态学特征。因此我们得出结论，磷脂代谢的改变以及肺表面活性剂合成减少和/或改变，至少在一定程度上在脓毒症和腹膜炎所致呼吸窘迫的发病机制中起重要作用。
