Oulton M, Moores H K, Scott J E, Janigan D T, Hajela R
Department of Physiology, Dalhousie University, Halifax, Nova Scotia, Canada.
Am J Pathol. 1991 Jan;138(1):195-202.
The effects of smoke inhalation on the pulmonary surfactant system were examined in mice exposed for 30 minutes to smoke generated from the burning of polyurethane foam. At 8 or 12 hours after exposure, surfactants were isolated separately from lung lavage (extracellular surfactant) and residual lung tissue (intracellular surfactant) for phospholipid analysis. Calcium-dependent phospholipase A2 (PLA2) was measured on a microsomal fraction prepared from the tissue homogenate. Smoke inhalation produced a twofold increase in extracellular surfactant total phospholipid. While there was no change in the total phospholipid or phosphatidylcholine (PC) content of the intracellular surfactant, smoke inhalation significantly decreased the disaturated species of PC (DSPC). The specific activity of PLA2 was reduced by more than 50% in both groups of exposed mice. Smoke inhalation appears to result in selective depletion of the DSPC of intracellular surfactant and PLA2 involved in its synthesis. This depletion may be compensated for by increased secretion or slower breakdown of the material present in the extracellular compartment.
在暴露于聚氨酯泡沫燃烧产生的烟雾中30分钟的小鼠身上,研究了吸入烟雾对肺表面活性物质系统的影响。暴露后8或12小时,分别从肺灌洗(细胞外表面活性物质)和残余肺组织(细胞内表面活性物质)中分离出表面活性物质进行磷脂分析。从组织匀浆制备的微粒体部分中测量钙依赖性磷脂酶A2(PLA2)。吸入烟雾使细胞外表面活性物质总磷脂增加了两倍。虽然细胞内表面活性物质的总磷脂或磷脂酰胆碱(PC)含量没有变化,但吸入烟雾显著降低了PC的二饱和物种(DSPC)。两组暴露小鼠的PLA2比活性均降低了50%以上。吸入烟雾似乎导致细胞内表面活性物质的DSPC及其合成过程中涉及的PLA2选择性耗竭。这种耗竭可能通过细胞外隔室中物质分泌增加或分解减慢来补偿。