| Abstract: | How does pulmonary emphysema affect aerosol deposition? Groups of awake hamsters with emphysema (intratracheal elastase, 0.2 mg/100 g body wt) and age-matched controls (intratracheal saline) were exposed for 30 minutes to an insoluble radioactive aerosol (0.45 mu aerodynamic diameter) at 30, 60, or 90 days after instillation. Immediately after exposure, the animals were sacrificed. The lungs were excised, dried at total lung capacity, and sliced into 1-mm thick sections. Each slice was cut into pieces, which were counted for radioactivity and weighed. Then a measure of the uniformity of deposition, the evenness index (EI), was calculated. With perfect uniformity, all EIs would be one. We found fewer particles in the emphysematous, as compared with the control, lungs at 60 or 90 days after elastase instillation. The deposited particles were distributed less uniformly throughout the emphysematous lungs than in the control lungs. In controls, the standard deviation (SD) of the EI distribution (mean 1.0) averaged 0.33 for the three times studied. In elastase animals, the SD increased to 0.48 at 30 days, and at 60 days and 90 days the distributions were no longer normally distributed. This increased heterogeneity of deposition was also manifested as a loss of the normal apex-base gradient observed in control animals, an increase in the amount of nonventilated parenchyma, enhanced airway deposition, and an altered lobar deposition pattern. Morphometric analysis showed an increase in the mean linear intercept (MLI) of emphysematous lungs as compared with control lungs. However, the author found no correlation between MLI, a measure of emphysema, and EI, a measure of deposition, quantified in the same lung pieces. It is concluded that the emphysematous lesions produced by elastase markedly alter the deposition of an inhaled submicrometric aerosol. Factors that may contribute to these changes include airway obstruction and differences in breathing pattern in emphysematous as compared with control animals. |
