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This Article Full Text Full Text (PDF) All Versions of this Article: 291/5/L1094    most recent 00180.2005v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in ISI Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via ISI Web of Science (4) Citing Articles via Google Scholar Google Scholar Articles by Azzam, Z. S. Articles by Abassi, Z. Search for Related Content PubMed PubMed Citation Articles by Azzam, Z. S. Articles by Abassi, Z.

Alveolar fluid reabsorption is increased in rats with compensated heart failure

¹Department of Physiology and Biophysics, Ruth & Bruce Rappaport Faculty of Medicine, Technion, Israel Institute of Technology; ²The Rappaport Family, Institute for Research in the Medical Sciences; ³Internal Medicine B; ⁵Department of Vascular Surgery and Transplantation, Rambam: Human Health Care Campus, Haifa, Israel; ⁴Division of Pulmonary and Critical Care Medicine, Columbia University, New York, New York; and ⁶Division of Pulmonary and Critical Care Medicine, Northwestern University, Chicago, Illinois

Submitted 21 April 2005 ; accepted in final form 22 June 2006

Alveolar fluid reabsorption (AFR) is important in keeping the air spaces free of edema. This process is accomplished via active transport of Na⁺ across the alveolo-capillary barrier mostly by apical Na⁺ channels and basolateral Na⁺-K⁺-ATPases. Recently, we have reported that acute elevation of left atrial pressures is associated with decreased AFR in isolated rat lungs. However, the effect of chronic elevation of pulmonary capillary pressure, such as seen in patients with congestive heart failure (CHF), on AFR is unknown. CHF was induced by creating an aorto-caval fistula (ACF) in Sprague-Dawley male rats. Seven days after the placement of the fistula, AFR was studied in the isolated perfused rat lung model. AFR in control rats was 0.49 ± 0.02 ml/h (all values are means ± SE) and increased by 40% (0.69 ± 0.03 ml/h) in rats with chronic CHF (P < 0.001). The albumin flux from the pulmonary circulation into the air spaces did not increase in the experimental groups, indicating that lung permeability for large solutes was not increased. Na⁺-K⁺-ATPase activity and protein abundance at the plasma membrane of distal alveolar epithelial tissue were significantly increased in CHF rats compared with controls. These changes were associated with increased plasma norepinephrine levels in CHF rats compared with controls. We provide evidence that in a rat model of chronic compensated CHF, AFR is increased, possibly due to increased endogenous norepinephrine upregulating active sodium transport and protecting against alveolar flooding.

edema; alveolar epithelium; Na⁺-K⁺-ATPase

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