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目的探讨门静脉性肺动脉高压(portopulmonary hypertension,PPHTN)犬肺动脉压力和肺血管超微结构。方法健康同龄同种系比格犬30只,随机分为PPHTN模型组和正常对照组,每组15只。模型组采取门静脉内注射葡聚糖微球栓塞制备PPHTN模型,成功建立模型后2、4、6、8、10、12周时,测量2组犬肺动脉压力,12周末取2组肺动脉行组织病理检查,观察2组犬肺动脉的超微结构,对肺血管的病理改变进行分级和图像计量学分析。结果 PPHTN模型组犬肺血管可见中膜增厚和动脉管壁肥厚等血管重构现象;PPHTN模型组犬肺动脉的肺小动脉中膜厚度[(111.41±41.05)mm]、肺小动脉密度[(4.51±1.61)μg/mm3]、血管壁面积/血管总面积[(80.80±7.99)%]及建模后12周肺动脉压力[(9.06±1.15)kPa]均明显高于对照组[(72.27±26.98)mm、(2.21±1.05)μg/mm3、(61.10±10.11)%、(1.53±0.89)kPa],差异有统计学意义(P<0.05)。结论 PPHTN犬肺动脉的超微结构可见血管重塑,肺动脉压力增高及血管内径减小是门脉性高压引起肺损伤的超微病理学基础,急性肺高压和急性肺损伤与门静脉高压存在密切关联。
Objective To investigate pulmonary arterial pressure and pulmonary vascular ultrastructure in portal hypertensive rats with portopulmonary hypertension (PPHTN). Methods Thirty healthy Beagle dogs of the same age were randomly divided into PPHTN model group and normal control group with 15 rats in each group. PPHNN model was established by embolization of dextran microspheres by portal vein in model group. Pulmonary arterial pressure was measured at 2, 4, 6, 8, 10 and 12 weeks after model establishment. At the end of 12 weeks, The ultrastructures of pulmonary arteries were observed and observed in two groups. The pulmonary vascular pathological changes were graded and imaged. Results The remodeling of pulmonary arteries in PPHTN model group was observed in the mediastinal thickening and arterial wall hypertrophy. The thickness of the pulmonary arterioles in the PPHTN model group [(111.41 ± 41.05) mm], pulmonary arteriole density [( 4.51 ± 1.61 μg / mm3], total wall area of blood vessel (80.80 ± 7.99%) and pulmonary artery pressure at 12 weeks after modeling (9.06 ± 1.15 kPa) were significantly higher than those in control group (72.27 ± (2.21 ± 1.05) μg / mm3, (61.10 ± 10.11)% and (1.53 ± 0.89) kPa, respectively), the difference was statistically significant (P <0.05). Conclusions The ultrastructure of pulmonary arteries in PPHTN can be seen in vascular remodeling, pulmonary hypertension and reduced vascular diameter is the pathological basis of lung damage caused by portal hypertension, acute pulmonary hypertension and acute lung injury and portal hypertension are closely related.