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J Thorac Cardiovasc Surg 2007;134:1213-1219
© 2007 The American Association for Thoracic Surgery
Cardiopulmonary Support and Physiology |
a Department of Thoracic Surgery, Kanazawa Medical University, Uchinada, Ishikawa, Japan
b Department of Pathology II, Kanazawa Medical University, Uchinada, Ishikawa, Japan.
Received for publication December 14, 2006; revisions received May 12, 2007; accepted for publication May 23, 2007. * Address for reprints: Tsutomu Sakuma, MD, PhD, Department of Thoracic Surgery, Kanazawa Medical University, Daigaku, Uchinada, Ishikawa 920-0293, Japan. (Email: sakuma-t{at}kanazawa-med.ac.jp).
Objective: 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.
Methods: 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 ß-adrenergic agonist and antagonist, mRNA expression, and protein expression in the lungs.
Results: 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 ß-agonist nor a ß-antagonist changed the increase in alveolar fluid clearance. Real-time polymerase chain reaction revealed an increase in
1-Na,K-ATPase mRNA and a decrease of ß2-adrenoreceptor mRNA, but no change in ß1-Na,K-ATPase mRNA and
-, ß-,
-epithelial sodium channel mRNA, in the left lung without pulmonary perfusion. Western blot analysis revealed an increase in
1-Na,K-ATPase subunit, but no change in ß1-Na,K-ATPase subunit.
Conclusion: Chronic pulmonary artery occlusion increases alveolar fluid clearance via
1-Na,K-ATPase overexpression in rats.
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