Objective:Impaired active fluid transport of al veolar epithelium may involve in the pathogenesis and resolution of alveolar ede ma. The objective of this study was to explore the changes in alveolar epithelia l liqui...Objective:Impaired active fluid transport of al veolar epithelium may involve in the pathogenesis and resolution of alveolar ede ma. The objective of this study was to explore the changes in alveolar epithelia l liquid clearance during lung edema following acute lung injury induced by olei c acid. Methods:Forty-eight Wistar rats were randomly divided into si x groups, i.e., injured, amiloride, ouabain, amiloride plus ouabain and terbutal ine groups. Twenty-four hours after the induction of acute lung injury by intra venous oleic acid ( 0.25 ml/kg), 5% albumin solution with 1.5 μCi 12 5 I-labeled albumin (5 ml/kg) was delivered into both lungs via trachea. Alveo lar liquid clearance (ALC), extravascular lung water (EVLW) content and arterial blood gases were measured one hour thereafter. Results:At 24 h after the infusion of oleic acid, the rats dev eloped pulmonary edema and severe hypoxemia, with EVLW increased by 47.9 % and ALC decreased by 49.2 %. Addition of either 2×10 -3 M amiloride or 5× 10 -4 M ouabain to the instillation further reduced ALC and increased E VLW. ALC increased by approximately 63.7 % and EVLW decreased by 46.9 % wi th improved hypoxemia in the Terbutaline (10 -4 M) group, compared those in injured rats. A significant negative correlation was found between the incremen t of EVLW and the reduction of ALC. Conclusions:Active fluid transport of alveolar epithelium migh t play a role in the pathogenesis of lung edema in acute lung injury.展开更多
文摘Objective:Impaired active fluid transport of al veolar epithelium may involve in the pathogenesis and resolution of alveolar ede ma. The objective of this study was to explore the changes in alveolar epithelia l liquid clearance during lung edema following acute lung injury induced by olei c acid. Methods:Forty-eight Wistar rats were randomly divided into si x groups, i.e., injured, amiloride, ouabain, amiloride plus ouabain and terbutal ine groups. Twenty-four hours after the induction of acute lung injury by intra venous oleic acid ( 0.25 ml/kg), 5% albumin solution with 1.5 μCi 12 5 I-labeled albumin (5 ml/kg) was delivered into both lungs via trachea. Alveo lar liquid clearance (ALC), extravascular lung water (EVLW) content and arterial blood gases were measured one hour thereafter. Results:At 24 h after the infusion of oleic acid, the rats dev eloped pulmonary edema and severe hypoxemia, with EVLW increased by 47.9 % and ALC decreased by 49.2 %. Addition of either 2×10 -3 M amiloride or 5× 10 -4 M ouabain to the instillation further reduced ALC and increased E VLW. ALC increased by approximately 63.7 % and EVLW decreased by 46.9 % wi th improved hypoxemia in the Terbutaline (10 -4 M) group, compared those in injured rats. A significant negative correlation was found between the incremen t of EVLW and the reduction of ALC. Conclusions:Active fluid transport of alveolar epithelium migh t play a role in the pathogenesis of lung edema in acute lung injury.
