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目的建立囊型包虫病肺梗塞的动物模型。方法取羊肝脏包虫囊内容物、分离出囊砂及澄清囊液,囊沙与囊液配成5％的混悬液。取21只家兔,随机分为三组:每组 n=7,Ⅰ组(生理盐水),Ⅱ组(澄清囊液),Ⅲ组(囊沙混悬液)。每只家兔均经股动静脉置入导管,依照上述分组按2 ml/kg 分别经静脉导管缓注生理盐水、澄清囊液、囊砂混悬液。于注射后5,10,30,60 min 取动脉血动态监测 MAP、血气指标。测定完成后经静脉缓注~(99m)Tc-MMA 2 ml,10 min 后扫描成像,观察结束后处死动物,取肺脏行光镜、电镜检查。结果Ⅲ组在注射后 MAP、血气均出现明显的降低,并低于Ⅰ组(P<0.05),而Ⅱ组虽有降低(P<0.05),但与Ⅲ组相比较下降程度小;ECT 显示Ⅲ组动物肺组织呈放射性缺损,Ⅱ组放射性减弱;病理:Ⅲ组可见头节广泛栓塞于肺小、微小动脉,呈“ARDS 样”改变,Ⅱ组表现为肺淤血、水肿及炎性细胞浸润。结论Ⅲ组动物基本能够模拟出囊型包虫病肺梗塞的临床表现,其中囊液中有形成分在肺梗塞中起主要作用。
Objective To establish an animal model of cystic echinococcosis with pulmonary infarction. Methods The contents of hydatid kidneys from sheep liver were taken out, and the cyst sand and clarified cyst fluid were separated. The cyst fluid and cystic fluid were dubbed as 5% suspension. Twenty - one rabbits were randomly divided into three groups: n = 7 in each group, group Ⅰ (normal saline), group Ⅱ (clear cyst fluid) and group Ⅲ (cystosa suspension). Each rabbit was catheterized by the femoral artery and vein, according to the above group by 2 ml / kg, respectively, by intravenous catheter slow saline, clarify the cyst fluid, cyst sand suspension. At 5, 10, 30, 60 min after injection, MAP and blood gas were monitored dynamically. After the measurement, intravenous infusion of ~ (99m) Tc-MMA 2 ml was given and scanned for imaging 10 minutes later. After the observation, the animals were sacrificed and the lungs were examined with light microscope and electron microscope. Results The levels of MAP and blood gas in group Ⅲ decreased significantly after injection and were lower than those in group Ⅰ (P <0.05), while those in group Ⅱ decreased (P <0.05) Ⅲ group of animals showed radioactive defect in the lung tissue, Ⅱ group decreased radioactivity; Pathology: Ⅲ group visible head section embolization in the small pulmonary arteries, showed “ARDS-like” changes, Ⅱ group showed pulmonary congestion, edema and inflammatory cell infiltration . Conclusion The animals in group Ⅲ can basically simulate the clinical manifestations of pulmonary embolism with cystic echinococcosis, in which the visible components of cystic fluid play a major role in pulmonary infarction.