Section Physiology, Department of Biomedical Sciences, University of Padova, Via Marzolo, 3, 35100, Padua, Italy,
Lung. 2013 Oct;191(5):459-66. doi: 10.1007/s00408-013-9488-y. Epub 2013 Jul 5.
This study was designed to investigate the possible effects of acute hyperbaric hyperoxia on respiratory mechanics of anaesthetised, positive-pressure ventilated rats.
We measured respiratory mechanics by the end-inflation occlusion method in nine rats previously acutely exposed to hyperbaric hyperoxia in a standard fashion. The method allows the measurements of respiratory system elastance and of both the "ohmic" and of the viscoelastic components of airway resistance, which respectively depend on the newtonian pressure dissipation due to the ohmic airway resistance to air flow, and on the viscoelastic pressure dissipation caused by respiratory system tissues stress-relaxation. The activities of inducible and endothelial NO-synthase in the lung's tissues (iNOS and eNOS respectively) also were investigated. Data were compared with those obtained in control animals.
We found that the exposure to hyperbaric hyperoxia increased respiratory system elastance and both the "ohmic" and viscoelastic components of inspiratory resistances. These changes were accompanied by increased iNOS but not eNOS activities.
Hyperbaric hyperoxia was shown to acutely induce detrimental effects on respiratory mechanics. A possible causative role was suggested for increased nitrogen reactive species production because of increased iNOS activity.
本研究旨在探讨急性高压高氧对麻醉、正压通气大鼠呼吸力学的可能影响。
我们通过终末充气阻断法测量了 9 只先前按标准方式急性暴露于高压高氧环境的大鼠的呼吸力学。该方法允许测量呼吸系统弹性和气道阻力的“欧姆”和粘弹成分，它们分别取决于牛顿对气流的气道阻力的耗散，以及由呼吸系统组织应力松弛引起的粘弹压力耗散。还研究了肺组织中诱导型和内皮型一氧化氮合酶的活性（分别为 iNOS 和 eNOS）。将数据与对照组动物的数据进行比较。
我们发现，高压高氧暴露增加了呼吸系统弹性和吸气阻力的“欧姆”和粘弹成分。这些变化伴随着 iNOS 活性的增加，但 eNOS 活性没有增加。
高压高氧急性诱导呼吸力学有害作用。由于 iNOS 活性增加，产生的氮反应性物质增加，可能起致病作用。
