摘要
【目的】观察门静脉和下腔静脉阻断与开放后门脉高压模型犬肺组织与肺动脉的病理学特点,从病理学角度初步探讨终末期肝硬化肝移植围术期急性肺高压和肺损伤的发生机制。【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)、对照组和门脉高压模型组(采用部分结扎门静脉的方法建立门脉高压症犬的模型并饲养12周),进行门静脉和肝后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,观察其病理形态学特征。【结果】模型组与对照组肺组织在经历门静脉和肝后下腔静脉阻断与开放后均存在不同程度病理形态学改变,但以模型组改变更为显著。门脉高压症犬肺小动脉密度、肺小动脉中膜厚度和血管壁面积/血管总面积(WA/TA)均显著大于阴性对照组和对照组;模型组的肺血管发生了以中膜增厚、动脉管壁肥厚为主要特征的血管重构现象。【结论】模型组犬易发生急性肺高压及肺损伤的特殊的病理学改变与存在门脉高压密切相关。
[Objective] To observe the pathological characteristic of lung and pulmonary artery after portal-cavity clamped and opened in portal hypertension canine, and investigate its mechanism of acute pulmonary hypertension and acute lung injury in order to explore orthotopic liver transplantation (OLT) inducing acute pulmonary hypertension and acute lung injury in the patients with final stage hepatic cirrhosis by pathological pathway, [Methods ] Eighteen canines were randomly divided into groups I (negative control group), Ⅱ (control group) and Ⅲ (model group), Canines in negative control group were only for collecting lung and pulmonary artery, and a partial ligation of portal vein were performed in model group. Experiment of portal-cavity clamped and opened was performed after 12 weeks in group Ⅱ and Ⅲ. Samples of lung and pulmonary artery were collected postoperatively, The pathological characteristic of lung and pulmonary arteries were analyzed, [Results] There were pathomorphological changes of pulmonary tissue after portal-cavity clamped and opened in group Ⅱ and Ⅲ. But it was more significant in group Ⅲ than it in the other groups. Density of small pulmonary artery, thickness of tunica media of small pulmonary artery and vessel wall area/ vessel total area (WA/TA) in group Ⅲ were significantly larger than the other groups. Vascular remodeling of pulmonary arteries was occurred in group Ⅲ, and its key features were thickening of tunica media and vessel wall of pulmonary artery. [Conclusion] From above data, we could conclude that pathological characteristic of acute pulmonary hypertension and lung injury cloud be related to existing portal venous hypertension in the model canines. But its mechanism should be further studied,
出处
《中山大学学报(医学科学版)》
CAS
CSCD
北大核心
2008年第2期144-148,共5页
Journal of Sun Yat-Sen University:Medical Sciences
基金
国家自然科学基金(30271254)
广东省科技计划项目(2004B35001005)
广东省自然科学基金(7001567)