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1 Department of Physiology and Biophysics, Ruth & Bruce Rappaport Faculty of Medicine, Technion, Israel Institute of Technology, Haifa, Israel; The Rappaport Family Institute for Research in the Medical Sciences, Haifa, Israel; Internal Medicine "B", Rambam: Human Health Care Campus, Haifa, Israel
2 Department of Physiology and Biophysics, Ruth & Bruce Rappaport Faculty of Medicine, Technion, Israel Institute of Technology, Haifa, Israel; Haifa, Israel
3 Division of Pulmonary and Critical Care Medicine, Northwestern University, Chicago, Illinois, United States
4 Chicago, Illinois, United States; Division of Pulmonary and Critical Care Medicine, Northwestern University, Chicago, Illinois, United States
5 Division of Pulmonary and Critical Care Medicine, Columbia University, New York, New York, United States
6 Department of Physiology and Biophysics, Ruth & Bruce Rappaport Faculty of Medicine, Technion, Israel Institute of Technology, Haifa, Israel; Internal Medicine "B", Rambam: Human Health Care Campus, Haifa, Israel
7 Department of Physiology and Biophysics, Ruth & Bruce Rappaport Faculty of Medicine, Technion, Israel Institute of Technology, Haifa, Israel; Vascular Surgery & Transplantation, Rambam: Human Health Care Campus, Haifa, Israel
* To whom correspondence should be addressed. E-mail: z_azzam{at}rambam.health.gov.il.
Background: Alveolar fluid reabsorption (AFR) is important in keeping the airspaces 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 of 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. Methods and Results: Chronic heart failure 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/hour (all values are mean ± SEM) and increased by ~40% (0.69±0.03 mL/hour) in rats with chronic CHF (p<0.001). The albumin flux from the pulmonary circulation into the airspaces 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 as compared as with controls. These changes were associated with increased plasma norepinephrine levels in CHF rats as compared to controls. Conclusions: We provide evidence that in a rat model of chronic compensated CHF; alveolar fluid reabsorption is increased, possibly due to increased endogenous norepinephrine upregulating active sodium transport and protecting against alveolar flooding.
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