血管紧张素转换酶Ⅱ在肺栓塞大鼠肺动脉中的表达及其对肺动脉血管的影响

Secretion and effects of angiotensin-converting enzyme 2 on pulmonary vascular remodeling in pulmonary embolism rats

目的通过观察肺栓塞大鼠肺动脉干、外周血中血管紧张素转化酶Ⅱ(ACE2)在栓塞发生后不同时间点的表达情况,分析其在肺动脉血管重构中的作用。方法将雄性SD清洁级大鼠120只按随机数字表法分为对照组、假手术和栓塞组,每组各40只。栓塞组大鼠再随机分为5个亚组,即栓塞24 h组、栓塞1周组、栓塞2周组、栓塞4周组和栓塞8周组。在相应的时间点进行肺动脉干、外周血中的ACE2含量检测及肺动脉干的病理检查。结果与对照组比较,假手术组大鼠肺动脉干、外周血中的ACE2的表达差异无统计学意义(P>0.05);栓塞组大鼠在栓塞1、2、4、8周后肺动脉干、外周血中的ACE2的表达均显著降低(P<0.05)。病理切片结果显示,栓塞组大鼠的肺动脉干出现明显的炎症细胞浸润、肺纤维化现象,并发生以肉芽组织增生为表现的血管重构现象。结论肺栓塞大鼠ACE2的表达明显降低;ACE2表达水平降低可能加重肺动脉血管重构。

Objective To measure angiotensin-converting enzyme 2 （ACE2） concentrations in peripheral blood and pulmonary artery trunk at different time points during the pulmonary embolism in rats, in order to investigate the effects of ACE2 on pulmonary vascular remodeling. Methods 120 male rats were randomly divided into pulmonary embolism group, control group and sham surgury group by random number table, with 40 rats in each group. Then, according to the different time points after embolization, the rats in puhnonary embolism group were further divided into 5 subgroups： embolization 24 h group, embolization 1 week group, embolization 2 weeks group, embolization 4 weeks group and embolization 8 weeks group. Concentrations of ACE2 both in pulmonary artery trunk and peripheral blood were measured at the corresponding time point, as well as the pathological examinations of pulmonary artery trunks. Results Compared with control group, the concentrations of ACE2 in the pulmonary trunk and peripheral blood of the sham operation group were not statistically significant （P 〉 0.05）. While the concentrations of ACE2 in pulmonary embolism group were significantly lower than those in control group at 1 week, 2 weeks, 4 weeks and 8 weeks after embolization （P 〈 0.01）. Meanwhile, pathological examination results showed clearly the infiltration of inflammatory ceils around pulmonary artery trunk, pulmonary fibrosis and vascular remod- eling with a hyperplasia of granulation tissue. Conelusion The expression of ACE2 reduced significantly in pulmonary embolism rat model, and the low con- eentrations of ACE2 may aggravate pulmonary vascular remodeling.