作者: Fouad Azizi , Abdelilah Arredouani , Ramzi M. Mohammad
DOI: 10.14814/PHY2.12453
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摘要: During airway inflammation, surface liquid volume (ASLV) expansion may result from the movement of plasma proteins and excess into lumen due to extravasation elevation subepithelial hydrostatic pressure. We previously demonstrated that submucosal pressure increases epithelium permeability resulting in ASLV by 500 μL cm−2 h−1. Liquid reabsorption healthy is regulated active Na+ transport at a rate 5 μL cm−2 h−1. Thus, during inflammation be submerged large luminal liquid. Here, we have investigated mechanism which alters epithelial transport, characterized time course change. used primary cultures tracheal maintained under air interface (basal ASLV, depth 7 ± 0.5 μm). To mimic flooding, was expanded 5 mm. On switching basal conditions, short-circuit current (Isc, measure total transepithelial ion transport) declined 90% with half-time (t1/2) 1 h. 24 h after switch, there no significant change ATP concentration nor number functional sodium pumps as revealed [3H]-ouabain binding. However, amiloride-sensitive uptake 22Na+ reduced 70% upon expansion. This process reversible since returning cells back interface, Isc recovered t1/2 5–10 h. These results important clinical implications concerning development channels activators resolution pulmonary edema.