[Relationship between alveolar epithelial type II cells and pulmonary surfactant protein A levels in young rats with acute lung injury].
OBJECTIVE
This study examined the relationship between the ultrastructural alterations of alveolar epithelial cells type II (AEC-II) and pulmonary surfactant protein A (SP-A) levels in the lung tissue of young rats with acute lung injury (ALI) in order to explore the possible mechanism of ALI.


METHODS
Forty-eight young Sprague-Dawley rats were randomly divided into control and ALI groups. The rats in the ALI group were intraperitoneally injected with 4 mg/kg of lipopolysaccharide (LPS) in order to induce ALI. The control subjects were injected with the same volume of normal saline. Rats were sacrificed at 24, 48 and 72 hrs after LPS or NS injection. Lung samples were obtained from the lower parts of the left lung and fixed with 2.5% glutaraldehyde for transmission electron microscope examination and for Western blot test of SP-A.


RESULTS
The microvilli of AEC-II disappeared 24 hrs after LPS injection. After 24 and 48 hrs of LPS injection, lamellar body (Lb) increased in number, enlarged in size and reduced in density, and the ring-like arrangement of Lb was present. By 48 hrs after LPS injection, giant Lb with vacuole-like deformity appeared. The contents of lung SP-A in the ALI group 24 hrs (6.52+/-0.62 vs 5.02+/-0.35; P<0.01) and 48 hrs (6.65+/-0.62 vs 5.01+/-0.36; P<0.01) after LPS injection were significantly higher than those in the control group. By 72 hrs after LPS injection, Lbs ruptured and were reduced in number. The shape of the nuclei was irregular and the border was blurred. The content of lung SP-A was greatly reduced in the ALI group 72 hrs after LPS injection compared with that in the control group (3.87+/-0.50 vs 5.22+/-0.36; P<0.01).


CONCLUSIONS
The alterations of AEC-II and lung SP-A were time-dependent in young rats with ALI induced by LPS. In the early stage of ALI, the lung SP-A content showed a compensatory increase. With the increasing injury of AEC-II cells, the secretion of SP-A presented with a decompensation and the lung SP-A content decreased. This may be one possible mechanism for the development of ARD.
Shu
Lin-Hua
LH
Department of Pediatrics, Shengjing Hospital, China Medical University, Shen-yang 110004, China.
Wei
Ke-Lun
KL
Shang
Yun-Xiao
YX
Wu
Hong-Min
HM
Li
Juan
J
Han
Xiao-Hua
XH
Cai
Xu-Xu
XX
Liu
Chun-Feng
CF
Li
Jiu-Jun
JJ
Wang
Li-Jie
LJ
Shi
Qi-Xing
QX
D000818:Animals; D005260:Female; D008070:Lipopolysaccharides / Q000633:toxicity; D008297:Male; D008854:Microscopy, Electron; D011650:Pulmonary Alveoli / Q000473:pathology* / Q000648:ultrastructure; D037662:Pulmonary Surfactant-Associated Protein A / Q000032:analysis*; D051381:Rats; D017207:Rats, Sprague-Dawley; D012128:Respiratory Distress Syndrome / Q000378:metabolism / Q000473:pathology*
D008070:Lipopolysaccharides; D037662:Pulmonary Surfactant-Associated Protein A