中文摘要：

目的观察门静脉和下腔静脉阻断与开放后门静脉高压模型犬肺组织与肺动脉的超微结构改变。方法正常家犬18只，随机均分为阴性对照组（仅用于取肺组织和肺动脉标本）、对照组和门静脉高压模型组（采用部分结扎门静脉的方法建立患门静脉高压症犬模型并饲养12周），进行门静脉、肝上和肝下下腔静脉阻断与开放实验。在术毕后取右下肺动脉和肺组织，应用透射电镜观察其超微结构。结果门静脉和下腔静脉阻断与开放后门静脉高压犬肺组织内皮细胞、Ⅰ型肺泡上皮细胞和Ⅱ型肺泡上皮均出现明显的病理性改变；肺泡隔纤维化明显，胶原纤维增生；肺毛细血管内血栓形成，基膜明显增厚；肺动脉血管内皮细胞损伤明显，部分脱落；肺动脉内皮细胞与中膜间隙明显增宽，内皮下水肿，内皮下胶原纤维增多。结论伴门静脉高压的肝移植犬肺组织和肺动脉的超微结构有明显改变，这可能是肝移植受者围术期出现急性肺高压和急性肺损伤的超微病理学基础之一。

英文摘要：

Objective To observe the uhrastructural pathological characteristics of pulmonary artery and lung in a portal hypertension canine model after portal and inferior vena cave clamped and opened and to preliminarily explore the mechanism of perioperative acute pulmonary hypertension and injury in liver transplantation for end-stage liver cirrhosis. Methods Eighteen canines were randomly divided into groups Ⅰ （negative control group）,Ⅱ （control group） and m （model group）. Canines in the negative control group were only for collecting lung and pulmonary artery, and a partial ligation of portal vein were performed in the model group. Portal-cavity was clamped and opened after 12 weeks in groups Ⅱ and Ⅲ. Samples of lung and pulmonary artery were collected postoperatively for transmission electron microscope observation. Results Endothelial cell, alveolar epithelial cell type Ⅰ and alveolar epithelium type Ⅱ showed obvious pathology changes ; alveolar septum developed fibrosis and collagen fiber proliferation; pulmonary capillary formed thrombosis, basal membrane thickened markedly. Pulmonary vascular endothelial cells were dramatically damaged and were shed in part; the gap between pulmonary artery endothelial cell and tunica media was widened and subendothelial edema and more collagen fiber were developed. Conclusions The uhrastructure of pulmonary artery and lung was obviously changed in a portal hypertension canine model. This may be the uhrastructural pathology basis for acute pulmonary hypertension and acute lung injury during the perioperation in liver transplantation.