Objective: To observe the changes of Na+-K+-ATPase activity in the lung tissue and the changes of ultra-structure in alveolar type Ⅱ cells in rats with lung defensive sluggishness syndrome(LDSS) and the regulation of rhubarb on it to explore the material foundation of LDSS and the mechanism of rhubarb in the prevention and treatment of the lung injury. Method: Lipopolysaccharide(LPS)was injected into SD rats to perform lung-defensive sluggishness syndrom

60 rats was randomizly divided into 5 groups:control group

lung-defensive sluggishness group

natural recovery after 5 days group

Rhubarb prevention group(9 g ·kg-1 ·d-1 for 2 days before modle establishment) and rhubarb treatment group(9 g ·kg-1 ·d-1 for 5 days after model establichment).The ultrastructure changes were observed under transmission electron microscope

The homogenate was used to detect the activity of Na+-K+-ATPase with the Na+-K+-ATPase kit. Result: Compared with the normal control group

alveolar type Ⅱ cells Lamellar body vacuoles

endoplasmic reticulum

cytoplasmic swelling and perinuclear extension were showed in the model group. A large number of alveolar type Ⅱ cells Lamellar body vacuoles

endoplasmic reticulum

markedly nuclear condensation were showed in the natural recovery after 5 days group. After the rhubarb intervention

the number of lamellar body of type Ⅱ cells was larger than that in recovery after 5 days group and lung-defensive sluggishness group

especially no enlargement of endoplasmic reticulum. It was showed that the expression of Na+-K+-ATPase activity of lung- defensive sluggishness group was lower than that of control group. However

the expression in the natural recovery after 5 days group was significant higher than control group. Rhubarb could inhibit the abnormal expression of Na+-K+-ATPase activity of lung. Conclusion: The abnormal ultra- structure of alveolar type Ⅱ cells and abnormal expression of Na+-K+-ATPase activity can be showed in lung-defensive sluggishness model and rhubarb can inhibit them

which is one of the important mechanisms for protecting the lung injury in lung-defensive sluggishness syndrome.