Journal
RESPIRATORY RESEARCH
Volume 15, Issue -, Pages -Publisher
BIOMED CENTRAL LTD
DOI: 10.1186/1465-9921-15-56
Keywords
Salbutamol; Acute respiratory distress syndrome; Elastance; Alveolar epithelial cells; Epithelial sodium channel; Edema
Categories
Funding
- personnel exchange grant (PROBRAL) of the Coordination for the Improvement of Higher Education Personnel (CAPES), Brasilia, Brazil
- German Academic Exchange Service (DAAD), Bonn, Germany
- Carlos Chagas Filho Rio de Janeiro State Research Foundation (FAPERJ), Rio de Janeiro, Brazil
- Brazilian Council for Scientific and Technological Development (CNPq), Brasilia, Brazil
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Introduction: We investigated the effects of intravenous and intratracheal administration of salbutamol on lung morphology and function, expression of ion channels, aquaporin, and markers of inflammation, apoptosis, and alveolar epithelial/endothelial cell damage in experimental pulmonary (p) and extrapulmonary (exp) mild acute respiratory distress syndrome (ARDS). Methods: In this prospective randomized controlled experimental study, 56 male Wistar rats were randomly assigned to mild ARDS induced by either intratracheal (n = 28, ARDSp) or intraperitoneal (n = 28, ARDSexp) administration of E. coli lipopolysaccharide. Four animals with no lung injury served as controls (NI). After 24 hours, animals were anesthetized, mechanically ventilated in pressure controlled mode with low tidal volume (6 mL/kg), and randomly assigned to receive salbutamol (SALB) or saline 0.9% (CTRL), intravenously (i.v., 10 mu g/kg/h) or intratracheally (bolus, 25 mu g). Salbutamol doses were targeted at an increase of approximate to 20% in heart rate. Hemodynamics, lung mechanics, and arterial blood gases were measured before and after (at 30 and 60 min) salbutamol administration. At the end of the experiment, lungs were extracted for analysis of lung histology and molecular biology analysis. Values are expressed as mean +/- standard deviation, and fold changes relative to NI, CTRL vs. SALB. Results: The gene expression of ion channels and aquaporin was increased in mild ARDSp, but not ARDSexp. In ARDSp, intravenous salbutamol resulted in higher gene expression of alveolar epithelial sodium channel (0.20 +/- 0.07 vs. 0.68 +/- 0.24, p < 0.001), aquaporin-1 (0.44 +/- 0.09 vs. 0.96 +/- 0.12, p < 0.001) aquaporin-3 (0.31 +/- 0.12 vs. 0.93 +/- 0.20, p < 0.001), and Na-K-ATPase-a (0.39 +/- 0.08 vs. 0.92 +/- 0.12, p < 0.001), whereas intratracheal salbutamol increased the gene expression of aquaporin-1 (0.46 +/- 0.11 vs. 0.92 +/- 0.06, p < 0.001) and Na-K-ATPase-a (0.32 +/- 0.07 vs. 0.58 +/- 0.15, p < 0.001). In ARDSexp, the gene expression of ion channels and aquaporin was not influenced by salbutamol. Morphological and functional variables and edema formation were not affected by salbutamol in any of the ARDS groups, regardless of the route of administration. Conclusion: Salbutamol administration increased the expression of alveolar epithelial ion channels and aquaporin in mild ARDSp, but not ARDSexp, with no effects on lung morphology and function or edema formation. These results may contribute to explain the negative effects of beta 2-agonists on clinical outcome in ARDS.
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