Pleural Cavity Exploitation in β-Agonist–treated ARDS Patients

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We read with great interest the article by Perkins and colleagues reporting that humans with ALI/ARDS receiving sustained treatment with intravenous -agonists exhibit acceleration in the clearance of alveolar edema (1). The need for a multicenter clinical trial is proposed to test the potential efficacy of the proposed therapy, with concomitant testing of the aerosolized delivery of the -agonist to achieve similar clinical efficacy and to avoid cardiac side effects. However, we believe that it would have been of interest for the authors to provide any data available regarding the occurrence of pleural effusions in the patients who underwent the BALTI trial. Leak of edema fluid into the pleural cavity in ARDS was suggested to represent an important route of interstitial edema clearance, acting as a safety factor with regard to alveolar flooding (2). In vivo studies in rabbits have shown that -adrenergic stimulation decreased by 25% the net rate liquid absorption of Ringer’s lactate hydrothoraces, while -adrenergic stimulation in the setting of 1% albumin-Ringer’s lactate hydrothoraces increased it by 29% (3). A recent study by our group, investigating the effect of adrenergic stimulation on pleural permeability in sheep, showed that stimulation of -adrenergic receptors results in reduction of the pleural permeability through Na transport inhibition (4). The effective concentrations of the -agonist used in the study of Zocchi and colleagues (5 10 6 M) (3), and by Zarogiannis and colleagues (10 7 M) (4) were similar and much higher than the concentration achieved in plasma when aerosolized -agonist is used as a therapeutic agent in patients with pulmonary edema (5). The findings that -adrenergic stimulation may inhibit or accelerate the absorption of excess pleural fluid from the pleural cavity, depending on the protein load, should be taken into account to achieve optimal alveolar and pleural clearance simultaneously in cases of ARDS complicated by pleural effusions. Such consideration might improve the effects on extravascular lung water as well as on pleural effusions as a clinical complication in ARDS.