| Summary: | In respiratory care involving situations of reduced lung function like that in disease or trauma, oxygen is given to relieve hypoxia. It is known that under certain conditions and prolonged exposure, oxygen is toxic to the lungs, the possible mechanisms being direct cellular damage or surfactant dysfunction. Physiological or clinical investigations into lung damage under different inhalant conditions are typically carried out over several hours or days, perhaps masking the
cause. We have developed a physiologically relevant experimental protocol to investigate changes in lung mechanics, with a high degree of sensitivity, based on indentation. This protocol takes advantage of the fact that, of all the internal organs, the lung has arguably the strongest correlation between mechanical behavior and physiologic function, or pathologies. The clinical focus of this work was to investigate possible changes in lung mechanics, and hence function when exposed to
100% oxygen for a duration equivalent only to several tidal volumes. Such short-term exposure would provide critical insight into the source of lung damage under oxygen environments. Three sets of experiments are presented here with the first test detailing macroscopic indents performed on inflated, excised lungs held under different physiologic conditions. Results from the indents prompted the development and implementation of a second set of experiments that combined indentation with
in situ microscopic observation of alveolar deformation, the first investigation of this kind. Macroscopic and microscopic observations were modeled using FEA and analytical methods to determine significant effects of oxygen on lung mechanics. The physiochemical origins of these mechanical differences were then explored by recourse to direct surface tension studies on the clinical surfactant formulation, Infasurf®, under various controlled environments
|
|---|
