国际儿科学杂志
國際兒科學雜誌
국제인과학잡지
INTERNATIONAL JOURNAL OF PEDIATRICS
2007年
3期
166-168,封3
,共4页
舒林华%薛辛东%舒林宏%刘春峰%吴红敏%韩晓华%尚云晓%蔡栩栩%许巍%魏克伦
舒林華%薛辛東%舒林宏%劉春峰%吳紅敏%韓曉華%尚雲曉%蔡栩栩%許巍%魏剋倫
서림화%설신동%서림굉%류춘봉%오홍민%한효화%상운효%채허허%허외%위극륜
脂多糖类%急性肺损伤%肺泡II型上皮细胞%肺表面活性蛋白
脂多糖類%急性肺損傷%肺泡II型上皮細胞%肺錶麵活性蛋白
지다당류%급성폐손상%폐포II형상피세포%폐표면활성단백
Lipopolysaccharide%Acute lung injury%Alveolar typeⅡcells%Surfacant prote
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.ATII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(4 mg/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、72 h随机处死每个亚组中8只幼鼠.于左肺下部取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,ATII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LB 48 h出现明显空泡变形,出现巨大LB,细胞核形态不规则.在48和72 h部分核边界不清.72 h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ATII细胞超微结构的改变是时间依赖性的.ATII细胞在48和72 h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.
目的 急性肺損傷和急性呼吸窘迫綜閤徵是兒科常見的和危害極大的疾病,病死率高達40%～70%.含有闆層小體(LB)的肺泡Ⅱ型(ATⅡ)上皮細胞可閤成和分泌肺錶麵活性物質,對維持肺內環境穩定和肺部免疫功能具有極其重要的意義.ATII上皮細胞的結構與其功能是相互協調一緻的.本研究的目的是研究脂多糖(LPS)誘導的急性肺損傷幼鼠肺泡Ⅱ型上皮細胞超微結構的變化.方法 腹腔內註射LPS(4 mg/kg)建立SD幼鼠急性肺損傷模型.正常對照組註射相同劑量的0.9%生理鹽水.分彆于註射後24、48、72 h隨機處死每箇亞組中8隻幼鼠.于左肺下部取1 mm3的肺組織固定于2.5%戊二醛中待透射電鏡檢查.結果 註射LPS 24 h後,ATII細胞微絨毛消失,LB數量增加,LB呈指環狀繞覈排列,細胞中有二箇細胞覈.細胞質中LB 48 h齣現明顯空泡變形,齣現巨大LB,細胞覈形態不規則.在48和72 h部分覈邊界不清.72 h細胞質中可見破碎及殘餘的LB,LB數目也明顯減少,部分細胞覈齣現覈溶解.結論 急性肺損傷時以LB、細胞覈、覈仁等的變化為主要特徵的ATII細胞超微結構的改變是時間依賴性的.ATII細胞在48和72 h破壞嚴重,這可能導緻肺錶麵活性物質閤成不足和肺動態平衡的不穩定,進而造成急性肺損傷.
목적 급성폐손상화급성호흡군박종합정시인과상견적화위해겁대적질병,병사솔고체40%～70%.함유판층소체(LB)적폐포Ⅱ형(ATⅡ)상피세포가합성화분비폐표면활성물질,대유지폐내배경은정화폐부면역공능구유겁기중요적의의.ATII상피세포적결구여기공능시상호협조일치적.본연구적목적시연구지다당(LPS)유도적급성폐손상유서폐포Ⅱ형상피세포초미결구적변화.방법 복강내주사LPS(4 mg/kg)건립SD유서급성폐손상모형.정상대조조주사상동제량적0.9%생리염수.분별우주사후24、48、72 h수궤처사매개아조중8지유서.우좌폐하부취1 mm3적폐조직고정우2.5%무이철중대투사전경검사.결과 주사LPS 24 h후,ATII세포미융모소실,LB수량증가,LB정지배상요핵배렬,세포중유이개세포핵.세포질중LB 48 h출현명현공포변형,출현거대LB,세포핵형태불규칙.재48화72 h부분핵변계불청.72 h세포질중가견파쇄급잔여적LB,LB수목야명현감소,부분세포핵출현핵용해.결론 급성폐손상시이LB、세포핵、핵인등적변화위주요특정적ATII세포초미결구적개변시시간의뢰성적.ATII세포재48화72 h파배엄중,저가능도치폐표면활성물질합성불족화폐동태평형적불은정,진이조성급성폐손상.
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.
