肺泡Ⅱ型上皮细胞对维持肺表面活性物质的动态平衡和肺免疫功能具有极其重要的意义。地塞米松对急性肺损伤肺泡Ⅱ型上皮细胞超微结构的影响目前仍不清楚。该研究探讨急性肺损伤时及应用地塞米松干预后肺泡Ⅱ型上皮细胞超微结构的动态变化。方法：72只21 d SD幼鼠随机分为对照组、急性肺损伤组和地塞米松治疗组。肺损伤组的幼鼠腹腔注射脂多糖(LPS)（4 mg/kg）以建立急性肺损伤模型。对照组注射等量生理盐水。地塞米松治疗组在注射LPS 1 h后腹腔注射地塞米松（5 mg/kg）。每组随机选取8只幼鼠分别于注射LPS或生理盐水后24、48、72 h处死。取左肺下1 mm3的肺组织固定于2.5% 戊二醛中待透射电镜检查。结果：注射LPS 24 h后，肺损伤组大鼠AT II细胞微绒毛消失，板层小体数量增加。24 及48 h 板层小体呈指环状绕核排列。48 h出现巨大空泡变性样的板层小体。细胞核形态不规则，部分核边界不清。72 h 板层小体数目明显减少,核仁从细胞核消失,一些细胞核出现核溶解。注射LPS 后24 h地塞米松治疗组板层小体聚集在AT II细胞内同侧，并于该侧发生“胞吐”现象。48 h线粒体肿胀、聚集，脊断裂， 板层小体数目减少。72 h板层小体数目增多，并重新呈指环状绕核排列。结论：LPS诱导的急性肺损伤肺泡Ⅱ型上皮细胞超微结构的一系列变化呈时间依赖性。地塞米松能减轻急性肺损伤中肺泡Ⅱ型上皮细胞损伤和促进肺泡Ⅱ型上皮细胞的功能恢复。［中国当代儿科杂志，2007，9（6）：521-525］

OBJECTIVE: Alveolar type II (AT II) cells play a crucial role in the maintenance of pulmonary surfactant homeostasis and pulmonary immunity. The effects of dexamethasone (Dex) on the ultrastructure of AT II cells after acute lung injury remain unknown. This study focused on the ultrastructural changes caused by acute lung injury and on the effects of Dex administration on these ultrastructural changes in young rats. METHODS: Seventy-two 21-day-old Sprague-Dawley rats were randomly divided into control, acute lung injury and Dex-treated groups. Rats in the lung injury group were intraperitoneally injected with 4 mg/kg lipopolysaccharide (LPS) in order to induce acute lung injury, while the control rats were injected with the same amount of normal saline (NS). The Dex-treated group was injected first with LPS followed 1hr later by Dex (5 mg/kg) injection. Eight rats in each group were sacrificed 24, 48 and 72 hrs after LPS or NS injection. Lung samples were obtained from the lower parts of left lungs and fixed with 2.5% glutaraldehyde for transmission electron microscope examination. RESULTS: Microvilli of AT II cells disappeared and the number of lamellar bodies (LBs) increased in the lung injury group 24 hrs after LPS injection. The ring-like arrangement of LBs around nuclei was present until 48 hrs after LPS injection. By 48 hrs after LPS injection, giant LBs with vacuole-like abnormalities appeared. The shape of nuclei became irregular and the border of the nuclei became blurred. By 72 hrs after LPS injection, the number of LBs was obviously reduced; nucleoli disappeared; and karyolysis occurred in some of the nuclei. In contrast, in the Dex-treated group, LBs crowded on one side of AT II cells and exocytosis appeared on the same side by 24 hrs after LPS injection. By 48 hrs, the number of LBs was reduced. The number of mitochondria increased, and some of them became swollen and enlarged. However, by 72 hrs, the number of LBs increased and the ring-like arrangement of LBs around the nucleus again appeared. CONCLUSIONS: Ultrastructural changes of AT II cells following lung injury induced by LPS were time-dependent in young rats. Dex may ameliorate AT II cell injury and promote functional restoration of AT II cells in LPS-induced acute lung injury. ［Chin J Contemp Pediatr, 2007, 9 (6):521-525］