Reduction in airway epithelial chloride transport in septicaemia related pulmonary oedema reversible by beta agonist application 英文参考文献.docVIP

Available online /content/10/3/412 Letter Reduction in airway epithelial chloride transport in septicaemia related pulmonary oedema reversible by beta agonist application Michael Eisenhut Paediatric Intensive Care Unit, Royal Liverpool Children’s Hospital, Eaton Road, Liverpool L12 2AP, United Kingdom Corresponding author: Michael Eisenhut, michael_eisenhut@ Published: 15 May 2006 Critical Care 2006, 10:412 (doi:10.1186/cc4916) This article is online at /content/10/3/412 ? 2006 BioMed Central Ltd See related research by Manocha et al., /content/10/1/R12 Manocha and colleagues [1] found in a retrospective study stimulation), which represents chloride channel function in on the association of beta-agonist use and lung injury a shorter duration and less severity of lung injury in patients on aerosolized beta-agonists. In their discussion of possible causes they and the investigators of the beta-agonist lung injury trial [2] did not comment on the effect of beta-agonist treatment on pulmonary chloride transport as an important independent determinant of pulmonary fluid clearance. It was first noted in experiments by Fang and colleagues [3] that the upper airway of children with meningococcal septicaemia related pulmonary oedema [6]. We found that nasal potential difference and amiloride response were not different between children with and without meningococcal septicaemia related pulmonary oedema. Response of the upper airway epithelium to a low chloride solution was, however, pulmonary oedema and this was significantly different to children ventilated for other forms of critical illness without absent in children with septicaemia related mice with inhibited or defective cystic fibrosis trans- membrane conductance regulator (CFTR) chloride channels (delta F508 homozygous) have a reduced cAMP depende