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Alveolar Epithelial Fluid Clearance Mechanisms Are Intact After Moderate Hyperoxic Lung Injury In Rats

Chrystelle Garat; Michel Meignan; Michael A. Matthay; Deng Feng Luo; Christian Jayr
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Affiliations: From the Departments of Physiology and Nuclear Medicine, Hôpital Henri Mondor, Institut National de la Santé et de la Recherche Médicale Unité 296, Créteil, France,  From the Departments of Medicine and Anesthesia and The Cardiovascular Research Institute, University of California, San Francisco,  From the Department of Anesthesia, Institut Gustave Roussy, Villejuif, France

Affiliations: From the Departments of Physiology and Nuclear Medicine, Hôpital Henri Mondor, Institut National de la Santé et de la Recherche Médicale Unité 296, Créteil, France,  From the Departments of Medicine and Anesthesia and The Cardiovascular Research Institute, University of California, San Francisco,  From the Department of Anesthesia, Institut Gustave Roussy, Villejuif, France

Affiliations: From the Departments of Physiology and Nuclear Medicine, Hôpital Henri Mondor, Institut National de la Santé et de la Recherche Médicale Unité 296, Créteil, France,  From the Departments of Medicine and Anesthesia and The Cardiovascular Research Institute, University of California, San Francisco,  From the Department of Anesthesia, Institut Gustave Roussy, Villejuif, France


1997 by the American College of Chest Physicians


Chest. 1997;111(5):1381-1388. doi:10.1378/chest.111.5.1381
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Abstract

The capacity of the alveolar epithelial barrier to remove excess alveolar fluid from the airspaces of the lung was studied in an experimental model of moderate hyperoxic lung injury. Rats were exposed to 100% oxygen for 40 h in an exposure chamber and compared with control animals exposed to room air. Extravascular lung water was calculated gravimetrically. Alveolar and lung liquid clearance were studied over 1 h by instillation of a 5% albumin solution with 1.5 µCi of 125I-labeled albumin (6 mL/kg into both lungs). The concentration of both the unlabeled and labeled albumin was used to calculate alveolar liquid clearance. Hyperoxic rats developed pulmonary edema, with a 33% increase in extravascular lung water to 5.3±0.1 g of water per gram of dry lung, compared with 4.0±0.2 g of water per gram of dry lung in control rats (p<0.05). This degree of edema was associated with a significant increase in the alveolar-arterial oxygen difference (241±61 vs 124±14 mm Hg in control animals exposed to room air, p<0.05). Despite this moderate degree of lung injury, alveolar fluid clearance was normal (30±3%) compared with control rats (33±6%). Furthermore, the hyperoxic injured rats responded normally to an exogenous β-adrenergic agonist (terbutaline, 10−4 mol/L) with a 67% increase in the rate of alveolar liquid clearance (50±5%). Thus, in the setting of moderate hyperoxic lung injury, the alveolar epithelial barrier is still capable of removing fluid at a normal rate and responding to β-adrenergic agonist treatment. These experimental results have potential clinical implications for patients with acute lung injury.


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