Hall S B, Lu R Z, Venkitaraman A R, Hyde R W, Notter R H
Department of Medicine, Oregon Health Sciences University, Portland 97201-3098.
J Appl Physiol (1985). 1992 May;72(5):1708-16. doi: 10.1152/jappl.1992.72.5.1708.
The inhibitory effects of oleic acid (OA) on the surface activity of pulmonary surfactant were characterized by use of the oscillating bubble surfactometer, the Wilhelmy balance, and excised rat lungs. Oscillating bubble studies showed that OA prevented lavaged calf surfactant [0.5 mM phospholipid (PL)] from lowering surface tension below 15 mN/m at or above a molar ratio of OA/PL = 0.5. In contrast to inhibition of surfactant by plasma proteins, increasing the surfactant concentration did not eliminate inhibition by oleic acid, which occurred at OA/PL greater than 0.67 on the oscillating bubble even at surfactant concentrations of 1.5 and 12 mM PL. Studies of surfactant adsorption showed that preformed films of OA had little effect on the adsorption of pulmonary surfactant. Wilhelmy balance studies showed that OA did interfere with the ability of spread films of surfactant to reach low surface tensions during dynamic compression. Further balance experiments with binary films of OA and dipalmitoyl phosphatidylcholine showed that these compounds were miscible in surface films. Together these findings suggested that OA inhibited pulmonary surfactant activity by disrupting the rigid interfacial film responsible for the generation of very low surface tension during dynamic compression. Mechanical studies in excised rat lungs showed that instillation of OA gave altered deflation pressure-volume characteristics with decreased quasi-static compliance, indicating disruption of pulmonary surfactant function in situ. This alteration of mechanics occurred without major changes in the composition of lavaged PLs or in the tissue compliance of the lungs defined by mechanical measurements during inflation-deflation with saline.(ABSTRACT TRUNCATED AT 250 WORDS)
通过使用振荡气泡表面活性剂测定仪、威廉米天平以及离体大鼠肺，对油酸（OA）对肺表面活性剂表面活性的抑制作用进行了表征。振荡气泡研究表明，在油酸与磷脂（PL）的摩尔比为0.5或更高时，油酸可阻止灌洗后的小牛表面活性剂[0.5 mM磷脂（PL）]将表面张力降低至15 mN/m以下。与血浆蛋白对表面活性剂的抑制作用不同，增加表面活性剂浓度并不能消除油酸的抑制作用，即使在表面活性剂浓度为1.5 mM和12 mM PL时，在振荡气泡上，当油酸与磷脂的摩尔比大于0.67时仍会出现抑制作用。表面活性剂吸附研究表明，预先形成的油酸膜对肺表面活性剂的吸附影响很小。威廉米天平研究表明，油酸确实会干扰表面活性剂铺展膜在动态压缩过程中达到低表面张力的能力。进一步用油酸和二棕榈酰磷脂酰胆碱的二元膜进行的天平实验表明，这些化合物在表面膜中是可混溶的。这些研究结果共同表明，油酸通过破坏在动态压缩过程中负责产生极低表面张力的刚性界面膜来抑制肺表面活性剂活性。对离体大鼠肺的力学研究表明，滴注油酸会改变放气压力-容积特性，准静态顺应性降低，表明原位肺表面活性剂功能受到破坏。这种力学改变在灌洗的磷脂组成或通过盐水充气-放气过程中的力学测量所定义的肺组织顺应性方面没有重大变化的情况下发生。（摘要截断于250字）
