Study On Sodium Transport In Alveolar Type Ⅱ Epithelial Cells Of ARDS Rats.

Objectives:In traditional theory, it is considered that development of pulmonary edemamainly as a result of the increase in hydrostatic pressure (cardiogenic edema) and capillary permeability (noncardiogenic edema). However, since Goodman found that alveolar epithelial cells could actively transport sodium ion, there were a lot of studies supported that the probable causes of lung edema included the disfunction of alveolar epithelial cells who could actively transport sodium ions, except for the 2 reasons mentioned before. Namely, the probable mechanisms of lung edema include"2 for increase, 1 for decrease ". The new mechanism which were found and validated to decrease lung liquid in order to maintain the balance of liquid across the alveolar epithelium will bring the traditional concept about origination of lung edema to a new milestone. Furthermore, what we had done before also proved the existence of "the third mechanism of lung edema", and we thought it would make a breakthrough at treatment of ARDS in clinic practice if we altered the function of the third pass.Alveolar epithelial cells, which constitute 95% of the alveolar surface area, consist of type I cells and type II cells. The junctions among epithelial cells mostly were Tight Junction that could limit water transport through epithelial cells, and it was propitious to the alveoli to remain free from fluid. Alveolar type II cells appear to play a momentous role in sodium transport, with the role of alveolar type I cells being...