细粒棘球蚴所致过敏性休克绵羊的肺部形态学观察

Morphological Observation on Lung of Sheep with Anaphylactic Shock Induced by Echinococcus granulosus

为观察细粒棘球蚴致过敏性休克绵羊肺部形态学的病理学和病理生理学变化 ,并探讨其发病机制 ,选用感染细粒棘球蚴的 12只绵羊 ,随机分为两组 ,Ⅰ组用细粒棘球蚴粗制囊液抗原 10mL攻击发敏 ,Ⅱ组用生理盐水作为对照组 ,确定休克的发生 ,实验观察 60min后处死绵羊 ,灌洗并收集支气管肺泡灌洗液并测定总蛋白 (TP)、红细胞 (RBC)、中性粒细胞(PMN)、巨噬细胞 (AM)含量 ,测定并计算绵羊肺湿 /干重量比值 ,分别观察绵羊肺部形态结构的变化。结果显示 ,Ⅰ组绵羊产生休克 ,在支气管肺泡灌洗液的测定中 ,实验组总蛋白含量、红细胞明显升高、中性粒细胞明显升高 ,巨噬细胞含量无明显变化 ,肺湿 /干重量比值明显升高。肺部形态结构观察 ,Ⅰ组均有明显早期肺损伤的病理变化。结论 :( 1)休克早期形成广泛的弥漫性蛋白通透性肺水肿 ;( 2 )肺部形态学改变特点为肺毛细血管淤滞、栓塞形成 ;( 3 )肺泡Ⅱ型细胞变性 ,肺表面活性物质分泌和转化异常是造成肺萎陷的主要原因 ;( 4 )炎细胞参与急性肺损伤的产生。

To observe the morphological changes of lung of sheep with anaphylactic shock induced by Echinococcus granulosus(E.g) and to approcah the mechanism, 12 sheep infected by E.g, were divided into experimental group (group I) and control group (groupⅡ) at random. Experimental group were challenged with E.g cystic fluid partially purified antigen 10mL by intrajugular injection to cause anaphylactic shock in sheep, while control group with sodium chloride injection 10mL. The anaphylactic shock was observed and confirmed after challenged, all of sheep were sacrificed after observation in 60 minutes. Bronchoalveolar lavage fluids were collected and the total protein, red blood cell, polymorphonuclear, alveolarmacrophage measured. Lung's rate of wet dry weight was measured. The morphological change of Lung of sheep was examined. After challenged, the sheep in experimental group occurred severe circulatory shock. In bronchoalveolar lavage fluid, total protein,red blood cell, polymorphonuclear of experimental group increased significantly compared with that in the control group and alveolarmacrophage was no changes. Lung rate of wet dry weight increased significantly of experimental group compared with that in the control group. Experimental group show obvious pathological changes while the control group was normal. (1) At early of shock, sheep of experimental group resulted from diffuse impairment of pulmonary endothelial cell, and protein rich edema in lung edema. (2) Characteristic of pathological changes was both widerspred embolism and silt of red blood cell in lung vascular. (3)Degeneration of large amounts of PⅡand abnormal secretion of the pulmonary surfactant appear to be the main factors contributing to atelectasis.(4) Accumulation of polymorphonuclear played an important role in acute lung injury.