RESUMO
Objective To study the temporal changes of alveolar epithelial type Ⅱ cells and surfactant pro-tein A in young rats with acute lung injury induced by lipopolysaecharide. Method Totally 110 SD young rats (male:53, female : 57) were randomly divided into ALI and normal control groups (six subgroups in each group).LPS(4 mg/kg) was given intraperitoneally in ALI group. The same amount of normal saline was given in the con-trol groups. Eight rats in each subgroup were sacrificed at 6, 12, 24, 36, 48 and 72 hours after the injection.Lung samples were taken for transmission electron microscope examination. RT-PCR was epmloyed for the mea-surement of SP-A mRNA. Western blot was used for the detection of SP-A in the lung tissue. ANOVA and homo-geneity of variance test were performed by SPSS 12.0. Results The microvilli disappeared at 24 hours after the injection of LPS. The number of lamellar body (LBs) was provisionality increased at 24 hours and 48 hours. The ring-like an'angement of LBs around nucleus and the giant LB with vacuole-like deformity were found as the main characteristics of AEC- Ⅱ in ALI at 48 hours. The number of LBs reduced and broken and residual LB remained at 72 hours. SP-A elevated greatly from 24 to 48 hours (P < 0.01), reached peak at 36 hours (6.94 ± 0.80, P <0.01),reached the lowest level(3.87 ±0.50, P <0.01)at 72 hours. Conclusions The pathological changes of AEC-Ⅱ and SP-A in lung tissue wiht ALI are time-dependent. The typical alterations of AEC- Ⅱ occurs at 48 hours accompanied by the compensatory increase of SP-A. AEC- Ⅱ is seriously injuried with the typical changes of LBs and the diminishing of SP-A in lung tissue.
RESUMO
Objective Acute lung injury (ALI) and acute respiratory distress syndrome (ARDS) are common and life-threatening disease in children with mortality as high as 40%-70%. Alveolar type Ⅱ cells (ATII cells),characterized by the presence of lamellar bodies (LBs),synthesize and secret surfactant proteins (SPs),which contribute significantly to surfactant homeostasis and pulmonary immunity.The functions of ATⅡ cells including pulmonary surfactant production are autocratically dominated by the structural integrity of ATII cells.Our study is focused on the ultrastructural alterations of AT Ⅱ cells in rats with lipopolysaccharide(LPS)-induced ALI.Methods Rat ALI models were established by intraperitoneal injection of LPS (4 mg/kg).0.9 % NS with same amount was given in the normal control group.The rats were randomly chosen and sacrificed at 24, 48 and 72 hrs after LPS injection (8 rats at each time point).Lung samples (1 mm3 of the size) were obtained from the lower parts of left lungs and fixed with 2.5% glutaraldehyde for the transmission electron microscope examination.Results The microvilli around ATII cells disappeared and the number of LBs increased at 24 hrs after LPS administration.LBs rearranged like a ring around the nuclei.It was commonly seen that two nuclei were present in one AT Ⅱ cell.Vacuole-like deformity prominently occurred in cytoplasm at 48 hrs.Giant LBs presented at the same time.The shapes of nuclei were irregular and some of the borders were unclear at 48 and 72 hrs.The remnant of ruptured LBs scattered in cytoplasm at 72 hrs.The number of LBs reduced obviously.Karyolysis occurred in some of the nuclei.Conclusions The ALI-related alterations of ATII cells characterized by the changes of LBs,nuclei,and nucleoli were time-dependent. ATII cell injury was serious at 48 and 72 hrs.This may lead to the insufficiency of pulmonary surfactant synthesis and unstability of pulmonary homeostasis,which contributed to to the pathogenesis of acute lung injury.