Indentation to Probe Atelectasis in Mammalian Lung
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0975-DD01-07
Indentation to Probe Atelectasis in Mammalian Lung Maricris C. Silva1, Melissa D. Hoyos1, Jean E. Rooney2, and Andrew Gouldstone1 1 Materials Science and Engineering, 130 Heavy Engineering, SUNY Stony Brook, Stony Brook, NY, 11794-2275 2 Laboratory Animal Resources, SUNY Stony Brook, Stony Brook, NY, 11794
ABSTRACT
Of all the internal organs, mechanical behavior of the lung is arguably most closely related to physiologic function. In inflation and deflation, lung parenchyma may be treated as an elastic material with some viscous damping. However, quasi-plasticity is observed, in the form of atelectasis, which is the localized collapse of alveoli under different conditions. General anesthesia in lung is known to increase tendency for pulmonary atelectasis, and this condition is typically removed by mechanical inflation to high pressures, which can be hazardous. The specific mechanisms of atelectasis are not fully known, one reason for this being the difficulty in developing a direct characterization method to perform causal investigations. In a previous abstract, we described the potential for controlled indentation tests to probe atelectatic tendency in lung. In this talk, we present the first results of 'hardness testing' on dog and rabbit lung, using different inflation schemes. Specifically, we indented excised lungs at physiologic pressures, inflated with air, pure oxygen, and 0.2% isoflurane in oxygen. Between these three conditions, we found marked differences in 'hardness' of the lung, when indented with tip radii comparable to that of ribs. That is to say, large contrasts in residual impressions, as well as re-inflation behavior, were observed. In addition, effects of different inflation gases occurred within a much shorter time than previously reported in other surgical experiments, indicating perhaps different, faster mechanisms controlling atelectasis than previously considered.
INTRODUCTION
Studies applying methods of continuum mechanics to non-uniform deformations of the lungs have previously been performed to investigate elastic properties of the lung [1,2]. However, although the presence of residual imprints from local indentation of the lungs was observed, plasticity, or quasi-plasticity in the lungs was never analyzed. These imprints may be described under the more general phenomenon of atelectasis, or alveolar collapse. In practice, atelectasis caused by general anesthesia or pulmonary disorders such as asthma and acute respiratory distress syndrome is treated by inflation of the lungs to high pressures and administration of high concentrations of oxygen to ensure adequate delivery of oxygen to the entire body. Both of these can be very harmful to the patient being treated, causing pathologies such as ventilator-induced lung injury or possible oxygen toxicity. In literature, the effects or manifestations of oxygen toxicity has been reported to occur 24 hours or more after exposure to high levels of oxygen (> 21% oxygen) where the higher the concentration of oxygen, the earlier the
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