Abstract
ObjectiveThe effect of IGF-1 in the human pleural permeability and the underlying mechanisms involved were investigated. DesignSpecimens from thoracic surgical patients were mounted in Ussing chambers. Solutions containing IGF-1 (1nM–100nM) and IGF-1 Receptor Inhibitor (1μΜ), amiloride 10μM (Na+ channel blocker) and ouabain 1mM (Na+–K+ pump inhibitor) were used in order to investigate receptor and ion transporter involvement respectively. Trans-mesothelial Resistance (RTM) across the pleural membrane was determined as a permeability indicator. Immunohistochemistry for IGF-1 receptors was performed. ResultsIGF-1 increased RTM when added on the interstitial surface for all concentrations (p=.008, 1nM–100nM) and decreased it on the mesothelial surface for higher concentrations (p=.046, 100nM). Amiloride and ouabain inhibited this effect. The IGF-1 Receptor Inhibitor also totally inhibited this effect. Immonuhistochemistry demonstrated the presence of IGF-1 receptors in the pleura. ConclusionsIt is concluded that IGF-1 changes the electrophysiology of the human parietal pleura by hindering the normal ion transportation and therefore the pleural fluid recycling process. This event is achieved after IGF-1 interaction with its receptor which is present in the human pleura.
Published Version
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call