首页> 美国卫生研究院文献>British Journal of Experimental Pathology >Changes in the Composition of Lung Lipids and the Turnover of Dipalmitoyl Lecithin in Experimental Alveolar Lipo-proteinosis Induced by Inhaled Quartz
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Changes in the Composition of Lung Lipids and the Turnover of Dipalmitoyl Lecithin in Experimental Alveolar Lipo-proteinosis Induced by Inhaled Quartz

机译:吸入石英诱导的实验性肺泡脂蛋白沉着症中肺脂质组成的变化和双棕榈酰卵磷脂的周转

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摘要

Specific pathogen-free rats, exposed to the inhalation of quartz for varying periods and surviving thereafter for several months, consistently developed alveolar lipo-proteinosis, but not typical silicosis as might have been expected. The overall lipid content of the lungs was much increased, notably the phospholipids and especially dipalmitoyl lecithin (DPL), whilst the lipid-free dry weight rose relatively little.In other rats, receiving brief but intenser exposures and surviving subsequently for a limited period so that the disease would be in an active phase, the rate of incorporation of labelled palmitic acid was measured and its rate of disappearance followed for 4 weeks. As compared with controls, the rate of synthesis of DPL was tripled and its rate of loss doubled. Accumulation of DPL in the lungs may thus be explained as an imbalance between formation and removal, though both are augmented. Our evidence conflicts with the view that the basic defect in alveolar lipo-proteinosis is a diminished capacity for elimination of alveolar secretion.The absolute plasma fatty acid content and the proportions of individual acids were unaffected in treated animals. It may therefore be concluded that the lipid accumulation derives from lung tissue rather than directly from the plasma, and type II epithelial cells appear to be a major source.
机译:特定的无病原体大鼠在不同时间段内接受石英吸入,然后存活数月,它们持续发展成肺泡脂蛋白沉着症,但并非典型的矽肺病。肺的总脂质含量大大增加,尤其是磷脂,尤其是二棕榈酰卵磷脂(DPL),而无脂质干重的增加相对较少。在其他大鼠中,短暂但强烈的暴露使之存活并因此在有限的时间内存活下来。疾病处于活动期,测量标记的棕榈酸的掺入速率,并在4周内追踪其消失速率。与对照相比,DPL的合成速率增加了三倍,其损失速率增加了一倍。肺中DPL的积累因此可以解释为形成和去除之间的不平衡,尽管两者都增加了。我们的证据与认为肺泡脂蛋白沉着的基本缺陷是消除肺泡分泌的能力降低的观点相矛盾。在治疗的动物中,血浆绝对脂肪酸含量和个别酸的比例不受影响。因此可以得出结论,脂质蓄积来自肺组织而不是直接来自血浆,并且II型上皮细胞似乎是主要来源。

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