Restoration of Pulmonary Functions after Reinflation in Chronic Atelectasis

Abstract

Recovery of the lungs after the reinflation of chronic atelectasis was studied experimentally using adult dogs. Obstructive absorption atelectasis was induced by banding the left main bronchus with a thin metallic plate. Tests were conducted 1 month after reinflation of the lungs. In the group of dogs which had suffered atelectasis for 3 months, static compliance and pulmonary blood flow were decreased by half at 1 month after reinflation; the conditions of reduced Po₂, increased A-aDo₂, and increased shunt flow rate in the affected lung persistently continued, and histological findings also showed collapse of the majority of alveoli and dilatation of the peripheral bronchioli, while macroscopically the lungs appeared to be aerated. It was therefore assumed that further aeration of the alveolar areas was impossible. The pulmonary function of the dogs within 1 month of atelectasis was restored to the same degree as that of the control group

Evaluation of pulmonary reexpansion in a porcine model of bronchial foreign body

“…Similarly, Ferrante et al made Yorkshire pig's right main stem bronchus plugging through a Fogarty‐catheter occlusion balloon inflation, and described atelectasis and its reexpansion using MRI in a few minutes. Harada et al established a dog model of pulmonary reexpansion after atelectasis by two thoracotomes and found that the pulmonary function of dogs within 1 month of atelectasis was restored to normal levels. However, the unilateral atelectasis in Harada's animal model, obtained by an aluminum plate flat pressing and sealing, was not suitable for simulating airway FB blockage.…”

Adverse effect of complete thoracic evacuation during chronic pneumothorax in a dog

“…Eventually, as the pneumothorax and the lung collapse worsen, ventilation is also impaired. Removal of the pleural air pocket will resolve the pneumothorax and should return normal pulmonary function (Harada et al. 1984; Padrid 2000).…”

“…The TLC can diminish with chronic pulmonary changes during pneumothorax. When the pneumothorax was resolved and the lung expanded the FRC and dead space increased providing little room for a normal tidal volume (Harada et al. 1984; Morris et al.…”

“…The TLC can diminish with chronic pulmonary changes during pneumothorax. When the pneumothorax was resolved and the lung expanded the FRC and dead space increased providing little room for a normal tidal volume (Harada et al 1984;Morris et al 1996;Kozower et al 2003). The lung and pleural elastic architecture is formed during the fetal and neonatal periods but pulmonary disease may result in damage to pulmonary elastin and replacement with collagen thus increasing FRC and dead space (Shapiro et al 1991;Pierce et al 1995;Billet & Sharpe 2002).…”

Lung Re-Expansion and Urinary Lipid Peroxidation in Neonatal Pneumothorax

“…The re-expansion of the collapsed lung in pneumothorax causes pulmonary edema and increases the amount of superoxide radicals [4]. Blood delivery to the collapsed lung significantly decreases and the decrease lasts longer than expected because of the hypoxic vasoconstriction [2]. The absence of alveolar ventilation during collapse leads to resorption of the air and consumption of the oxygen by alveolar endothelial and epithelial cells.…”