Early administration of propofol protects against endotoxin-induced acute lung injury in rats by inhibiting the TGF-beta1-Smad2 dependent pathway.

Objective: To assess the effects of propofol treatments at different time points on acute lung injury and on the expression of transforming growth factor (TGF)-beta1 and the downstream target of TGF-beta1, Smad 2, in the lung tissues in the endotoxic rats.

Methods: Seventy-six Wistar rats were randomly assigned to five groups: control group (saline only), endotoxemic group [lipopolysaccharide (LPS) 8 mg kg(-1), i.v.

[Effects of different fluid resuscitation regimes on lung injury and expression of pulmonary aquaporin 1 and aquaporin 5 in uncontrolled hemorrhagic shock in rats].

Objective: To investigate the effects of different fluid resuscitation regimes on lung injury and expression of pulmonary aquaporin 1 (AQP1) and AQP5 in rats with uncontrolled hemorrhagic shock.

Methods: Sixty Sprague-Dawley (SD) rats were randomly assigned to the following five groups: control group (C group), no fluid resuscitation group (NF group), lactated Ringer's solution group (LRS group), 7.5%NaCl group (HS group) and hydroxyethyl starch group (hydroxyethyl starch 130/0.

[Changes in pulmonary transforming growth factor-beta1/smad2 signaling pathway in a two-hit pulmonary injury as a result of uncontrolled hemorrhagic shock and lipopolysaccharide in rats].

Objective: To investigate the changes in pulmonary transforming growth factor-beta1 (TGF-beta1)/smad2 signaling pathway in pulmonary injury as a result of hemorrhagic shock followed by lipopolysaccharide challenge.

Methods: Twenty-four Sprague-Dawley (SD) rats were randomly assigned to the following two groups: sham operation group (sham group, surgery, no hemorrhage and no resuscitation), and two-hit model group (HS group), each n=12. Three-phased uncontrolled hemorrhagic shock model was reproduced in rats.