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Articles in PresS, published online ahead of print February 22, 2002
Am J Physiol Lung Cell Mol Physiol, 10.1152/ajplung.00089.2000
Submitted on March 7, 2000
Accepted on January 10, 2002
1 Department Enfermedades Respiratorias, Pontificia Universidad Catolica de Chile, Santiago, Chile
2 Pulmonary and Critical Care Medicine, Northwestern University, Chicago, Ill, USA
* To whom correspondence should be addressed. E-mail: j-sznajder{at}nwu.edu.
Short term mechanical ventilation with high tidal volume (HVT) causes mild to moderate lung injury and impairs active Na+ transport and lung liquid clearance in rats. Dopamine (DA) enhances active Na+ transport in normal rat lungs by increasing Na,K-ATPase activity in the alveolar epithelium. We examined whether DA would increase alveolar fluid reabsorption in rats ventilated with HVT for 40 min as compared to low tidal volume (LVT) and non-ventilated rats. Similar to previous reports, HVT ventilation decreased alveolar fluid reabsorption by ~50% (p<0.001). Dopamine increased alveolar fluid reabsorption in non-ventilated control rats (by ~60%), LVT ventilated rats (by ~55%) and HVT ventilated rats (by ~200%). In parallel studies, DA increased Na,K-ATPase activity in cultured rat alveolar epithelial type II cells (ATII). Depolymerization of cellular microtubules by colchicine inhibited the effect of dopamine on HVT ventilated rats as well as on Na,K-ATPase activity in ATII cells. Neither dopamine nor colchicine did affect the short term Na,K-ATPase
1- and ß1-subunit mRNA steady state levels or total
1- and ß1-subunit protein abundance in ATII cells. Thus, we reason that dopamine improved alveolar fluid reabsorption in rats ventilated with HVT by upregulating the Na,K-ATPase function in alveolar epithelial cells.
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