摘要
目的急性肺损伤和急性呼吸窘迫综合征是儿科常见的和危害极大的疾病，病死率高达40％-70％。含有板层小体（LB）的肺泡Ⅱ型（ATⅡ）上皮细胞可合成和分泌肺表面活性物质，对维持肺内环境稳定和肺部免疫功能具有极其重要的意义。ATH上皮细胞的结构与其功能是相互协调一致的。本研究的目的是研究脂多糖（LPS）诱导的急性肺损伤幼鼠肺泡Ⅱ型上皮细胞超微结构的变化。方法腹腔内注射LPS（4mg/kg）建立SD幼鼠急性肺损伤模型。正常对照组注射相同剂量的0．9％生理盐水。分别于注射后24、48、72h随机处死每个亚组中8只幼鼠。于左肺下部取1mm^3的肺组织固定于2．5％戊二醛中待透射电镜检查。结果注射LPS24h后，ATH细胞微绒毛消失，LB数量增加，LB呈指环状绕核排列，细胞中有二个细胞核。细胞质中LB48h出现明显空泡变形，出现巨大LB，细胞核形态不规则。在48和72h部分核边界不清。72h细胞质中可见破碎及残余的LB，LB数目也明显减少，部分细胞核出现核溶解。结论急性肺损伤时以LB、细胞核、核仁等的变化为主要特征的ATH细胞超微结构的改变是时间依赖性的。ATH细胞在48和72h破坏严重，这可能导致肺表面活性物质合成不足和肺动态平衡的不稳定，进而造成急性肺损伤。
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 （ATI/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 ATH cells including pulmonary suffactant production are autocratically dominated by the structural integrity of ATH tells. Our study is focused on the ultrastructural alterations of AT Ⅱ cells in rats with lipopolysaochafide（LPS）-induced ALI.Methods Rat ALI models were established by intraperitOneal injection of LPS （4mg/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 mm^3 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 ATH 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-llke 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 ATH cells characterized by the changes of LBs, nuclei, and nucleoli were timedependent. ATH cell injury was serious at 48 and 72 hrs. This may lead to the insufficiency of pulmonary surfaetant synthesis and unstability of pulmonary homeostasis, which contributed to to the pathogenesis of acute lung injury.
出处
《国际儿科学杂志》
2007年第3期166-168,F0003,共4页
International Journal of Pediatrics
