Fuortes M, Pollock T W, Holman M J, McMillen M A, Jaffe B M, Scalea T M
Department of Surgery, SUNY Health Science Center, Brooklyn 11203.
J Trauma. 1988 Oct;28(10):1455-9. doi: 10.1097/00005373-198810000-00008.
Several mediators, including fatty acids, have been postulated to induce the increase in permeability of the pulmonary endothelium and subsequent accumulation of extravascular lung water (EVLW) which are generally considered to be among the first events in the development of adult respiratory distress syndrome. In a canine model of hyperdynamic sepsis (hemodynamically similar to human sepsis) changes in EVLW and in concentrations of different fatty acids in the aortic and pulmonary arterial blood were measured. Two days after induction of sepsis, EVLW increased from 6.6 +/- 0.6 to 9.2 +/- 1.0 ml/kg, and the pulmonary arterial concentration of oleic acid increased from 52 +/- 4 to 73 +/- 5 mg/dl. Three days after induction of sepsis, EVLW increased further to 14.4 +/- 3.8 ml/kg and the mean concentration of oleic acid increased to 74 +/- 7 mg/dl. Twenty-four hours later, both EVLW and the mean pulmonary arterial concentration of oleic acid were not different from basal. We postulate that oleic acid, a known inducer of experimental ARDS, is one of the mediators of endothelial damage of the lung during sepsis.
包括脂肪酸在内的多种介质被认为可诱导肺内皮通透性增加以及随后血管外肺水(EVLW)的蓄积,而这些通常被视为成人呼吸窘迫综合征发生过程中的早期事件。在一个高动力性脓毒症犬模型(血流动力学与人类脓毒症相似)中,测量了EVLW以及主动脉和肺动脉血中不同脂肪酸浓度的变化。脓毒症诱导后两天,EVLW从6.6±0.6增加至9.2±1.0 ml/kg,肺动脉油酸浓度从52±4增加至73±5 mg/dl。脓毒症诱导后三天,EVLW进一步增加至14.4±3.8 ml/kg,油酸平均浓度增加至74±7 mg/dl。24小时后,EVLW和肺动脉油酸平均浓度均与基础值无差异。我们推测,油酸作为实验性ARDS的已知诱导剂,是脓毒症期间肺内皮损伤的介质之一。