中国现代医学杂志
中國現代醫學雜誌
중국현대의학잡지
CHINA JOURNAL OF MODERN MEDICINE
2005年
18期
2739-2742,2753
,共5页
周学武%尚涛%唐颖%杜少敏%冯丽艳
週學武%尚濤%唐穎%杜少敏%馮麗豔
주학무%상도%당영%두소민%풍려염
羊水栓塞%肺损伤%补体
羊水栓塞%肺損傷%補體
양수전새%폐손상%보체
amniotic fluid embolism(AFE)%pulmonary injury%complement%myeloperoxidase(MPO)
目的探讨鼠羊水栓塞后肺病理变化及补体的作用.方法精选雄性Wistar大鼠30只于妊娠20d制作羊水栓塞模型.根据注入液体性质不同随机分为对照组(10只)、羊水组(10只)、胎粪液组(10只).对照组除注入生理盐水外,皆同其余组.实验后取大鼠左肺行HE染色光镜下观察,右肺行MPO检查,免疫比浊法测各组前后的补体C3、C4水平.结果实验组肺组织可见大量炎性细胞浸润,包括白细胞(主要为中性粒细胞)、巨噬细胞及少量淋巴细胞;MPO含量明显升高,差异显著.生理盐水组注入前后补体C3、C4水平无明显差异(P>0.05);鼠原羊水组和胎粪液组注入前后补体C3、C4水平明显降低,差异显著(P<0.01).结论补体系统在羊水栓塞中被大量激活、消耗,其活化裂解产生的片段引起中性粒细胞、巨噬细胞浸润及一系列病理变化,由此引起肺损伤及临床症状.
目的探討鼠羊水栓塞後肺病理變化及補體的作用.方法精選雄性Wistar大鼠30隻于妊娠20d製作羊水栓塞模型.根據註入液體性質不同隨機分為對照組(10隻)、羊水組(10隻)、胎糞液組(10隻).對照組除註入生理鹽水外,皆同其餘組.實驗後取大鼠左肺行HE染色光鏡下觀察,右肺行MPO檢查,免疫比濁法測各組前後的補體C3、C4水平.結果實驗組肺組織可見大量炎性細胞浸潤,包括白細胞(主要為中性粒細胞)、巨噬細胞及少量淋巴細胞;MPO含量明顯升高,差異顯著.生理鹽水組註入前後補體C3、C4水平無明顯差異(P>0.05);鼠原羊水組和胎糞液組註入前後補體C3、C4水平明顯降低,差異顯著(P<0.01).結論補體繫統在羊水栓塞中被大量激活、消耗,其活化裂解產生的片段引起中性粒細胞、巨噬細胞浸潤及一繫列病理變化,由此引起肺損傷及臨床癥狀.
목적탐토서양수전새후폐병리변화급보체적작용.방법정선웅성Wistar대서30지우임신20d제작양수전새모형.근거주입액체성질불동수궤분위대조조(10지)、양수조(10지)、태분액조(10지).대조조제주입생리염수외,개동기여조.실험후취대서좌폐행HE염색광경하관찰,우폐행MPO검사,면역비탁법측각조전후적보체C3、C4수평.결과실험조폐조직가견대량염성세포침윤,포괄백세포(주요위중성립세포)、거서세포급소량림파세포;MPO함량명현승고,차이현저.생리염수조주입전후보체C3、C4수평무명현차이(P>0.05);서원양수조화태분액조주입전후보체C3、C4수평명현강저,차이현저(P<0.01).결론보체계통재양수전새중피대량격활、소모,기활화렬해산생적편단인기중성립세포、거서세포침윤급일계렬병리변화,유차인기폐손상급림상증상.
[Objective] To evaluate the pathological change of pulmonary and role of complement in amniotic fluid embolism after laboring in rats. [Methods] Strictly selected 30 Wistar rats(late pregnancy) and randomly diyided into the control group, amniotic fluid group, and meconium fluid group. The procedure for control group was exactly the same as the experimental groups except injecting NS. After experimented, the left lung of the rat was perfused with 10% Formalin, H.E, the right lung of the rat was taken for the activity of MPO examination, main outcome measures were complement levels (C3 and C4). [Results] There were lots of infiltration of neutrophil and macrophage in pulmonary tissue of experimental groups. MPO was significantly higher in experimental groups. There were no change of complement levels in control group (P >0.05); All experimental groups had abnormally low level of complement, compared with before infusion values(P <0.01). [Conclusions] These results suggest that the activation of complement was probably the potential initial factor which could further lead to AFE and multiple organ dysfunction syndrome (MODS). Laboratory data suggest that massive activation of the complement has an important role in the pathophysiology of the disease.