| dc.description.abstract | Aim: Insulin promotes ion transportation across epithelia, mainly kidneys, leading to water and electrolyte abnormalities, possibly causing 'insulin oedema syndrome', which rarely presents as pleural effusion. Direct stimulation of sheep pleura by insulin and the possible electrophysiology mechanisms involved were investigated. Material and Methods: Sheep visceral and parietal pleural specimens were mounted between Ussing chambers. Insulin solutions (10(-9) to 10(-5) M), L-NAME, Nitroprussid sodium, amiloride and ouabain were used. Trans-mesothelial Resistance was determined. Immunohistochemistry for presence of Insulin Receptors was performed. Results: Insulin increased Trans-mesothelial Resistance within 1st minute when added mesothelially of visceral (p = 0.008) and parietal pleura (p = 0.046) for concentrations higher than 10(-7) M. L-NAME or Nitroprussid sodium didn't but amiloride and ouabain inhibited insulin's effect. Immunohistochemistry revealed the presence of Insulin Receptors. Conclusion: Insulin changes the permeability of sheep pleura by altering its electrophysiology and may interfere in pleural effusion formation. Involvement of Insulin Receptors may be suggested. | en |
