Abstract

We had observed that pulmonary artery ligation for 14 days did not induce lung infiltration in a patient who had undergone a lobectomy for lung cancer. Our hypothesis was that long-term pulmonary artery ligation decreased lung water volume and/or increased alveolar fluid clearance. We determined the mechanism responsible for lung water balance in rats with chronic pulmonary artery occlusion for 14 days. Sprague-Dawley rats (n = 45) were used. Through a left thoracotomy, the left pulmonary artery was ligated for 14 days. Then, we measured lung water volume, alveolar fluid clearance, the effects of beta-adrenergic agonist and antagonist, mRNA expression, and protein expression in the lungs. Chronic left pulmonary artery occlusion increased both lung water volume and alveolar fluid clearance in the left lungs, but not in the right lungs with pulmonary perfusion. Neither a beta-agonist nor a beta-antagonist changed the increase in alveolar fluid clearance. Real-time polymerase chain reaction revealed an increase in alpha1-Na,K-ATPase mRNA and a decrease of beta2-adrenoreceptor mRNA, but no change in beta1-Na,K-ATPase mRNA and alpha-, beta-, gamma-epithelial sodium channel mRNA, in the left lung without pulmonary perfusion. Western blot analysis revealed an increase in alpha1-Na,K-ATPase subunit, but no change in beta1-Na,K-ATPase subunit. Chronic pulmonary artery occlusion increases alveolar fluid clearance via alpha1-Na,K-ATPase overexpression in rats.

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