title: Alveolar fluid reabsorption is increased in rats with compensated heart failure.
abstract: 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 approximately 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.
authors.affiliation: Department of Physiology and Biophysics, Ruth & Bruce Rappaport Faculty of Medicine, Technion, Israel Institute of Technology. z_azzam@rambam.health.gov.il
authors.forename: Zaher S
authors.initials: ZS
authors.lastname: Azzam
authors.forename: Yochai
authors.initials: Y
authors.lastname: Adir
authors.forename: Lynn
authors.initials: L
authors.lastname: Welch
authors.forename: Jiwang
authors.initials: J
authors.lastname: Chen
authors.forename: Joseph
authors.initials: J
authors.lastname: Winaver
authors.forename: Phillip
authors.initials: P
authors.lastname: Factor
authors.forename: Norberto
authors.initials: N
authors.lastname: Krivoy
authors.forename: Aaron
authors.initials: A
authors.lastname: Hoffman
authors.forename: Jacob I
authors.initials: JI
authors.lastname: Sznajder
authors.forename: Zaid
authors.initials: Z
authors.lastname: Abassi
mesh_terms: D000315:Adrenalectomy; D000319:Adrenergic beta-Antagonists / Q000494:pharmacology; D000584:Amiloride / Q000494:pharmacology; D000818:Animals; D002302:Cardiac Output; D004195:Disease Models, Animal; D004232:Diuretics / Q000494:pharmacology; D004837:Epinephrine / Q000378:metabolism; D015633:Extravascular Lung Water / Q000378:metabolism*; D006333:Heart Failure / Q000188:drug therapy / Q000378:metabolism* / Q000473:pathology; D007150:Immunohistochemistry; D008297:Male; D009206:Myocardium / Q000473:pathology; D009638:Norepinephrine / Q000378:metabolism; D009929:Organ Size; D011433:Propranolol / Q000494:pharmacology; D011650:Pulmonary Alveoli / Q000378:metabolism* / Q000473:pathology; D011654:Pulmonary Edema / Q000188:drug therapy / Q000378:metabolism* / Q000473:pathology; D051381:Rats; D017207:Rats, Sprague-Dawley; D000254:Sodium-Potassium-Exchanging ATPase / Q000378:metabolism; D017725:Ventricular Pressure
chemical_list: D000319:Adrenergic beta-Antagonists; D004232:Diuretics; D000584:Amiloride; D011433:Propranolol; D000254:Sodium-Potassium-Exchanging ATPase; D009638:Norepinephrine; D004837:Epinephrine