کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
2847059 | 1571333 | 2014 | 10 صفحه PDF | دانلود رایگان |
• Longer duration pneumothorax exacerbated epithelial cell damage yielding oedema.
• Mechanism of oedema formation is related to an imbalance between water channels.
• Early compared to late PTX drainage yielded less oedema and higher CFTR expression.
We analyzed the effects of pneumothorax duration and early or late drainage on lung histology and biological markers associated with inflammation, alveolar fluid clearance, and pulmonary oedema formation. Pneumothorax was induced by injecting air into the thorax of anaesthetized rats, which were randomized according to duration of pneumothorax [5 (PTX5) or 30 (PTX30) min] and further divided to be drained (D) or not (ND). ND rats were euthanized at 5 and 30 min. In D groups, pneumothorax was drained and rats breathed spontaneously for 30 min. PTX30-ND, compared to PTX5-ND, showed higher alveolar collapse and oedema, type III procollagen, caspase-3, epithelial sodium channel-α, and aquaporin (AQP)-1 mRNA expression, and epithelial and endothelial damage, with reduced cystic fibrosis transmembrane conductance regulator (CFTR) and AQP-3 expression. PTX5-D, compared to PTX30-D, showed less alveolar hyperinflation, oedema, and alveolar-capillary damage, with reduced interleukin-6, caspase-3, AQP-5, and Na,K-ATPase-α and -β expression, and increased CFTR expression. In conclusion, longer duration pneumothorax exacerbated lung damage, oedema, and inflammation.
Journal: Respiratory Physiology & Neurobiology - Volume 195, 1 May 2014, Pages 27–36