肺动脉血管紧张素转换酶在缺氧性肺动脉高压演进过程中的作用

Role of pulmonary arterial angiotensin converting enzyme in development of hypoxic pulmonary hypertension

目的探讨肺动脉局部肾素－血管紧张素系统对缺氧性肺动脉高压（ＰＡＨ）的影响。方法采用常压缺氧ＰＡＨ动物模型，观察缺氧后肺动脉收缩压（ＰＡＰｓ）、肺动脉血管紧张素转换酶（ＡＣＥ）活性、胶原蛋白含量（Ｈｐ）及血管平滑肌细胞（ＳＭＣ）超微结构的变化，以及ＡＣＥ抑制剂－西拉普利对以上变化的影响。结果缺氧期间ＰＡＰｓ、ＡＣＥ活性、Ｈｐ显著增高，ＳＭＣ转为分泌型。西拉普利组ＡＣＥ活性下降，ＰＡＰｓ、Ｈｐ降至正常，ＳＭＣ恢复收缩表型。结论肺动脉ＡＣＥ参与缺氧性ＰＡＨ形成、转归过程中肺动脉胶原代谢、ＳＭＣ表型变化的调节。

Objective To study the effect of local pulmonary arterial renin angiotensin system on hypoxic pulmonary hypertension(PAH). Methods Normobaric hypoxic PAH animal model was adopted.Systolic pulmonary arterial pressure(PAPs), pulmonay arterial angiotensin converting enzyme(ACE) activity, collagen content(HP) were measured and ultrastructure of pulmonary smooth muscle cells(SMC) and was observed.Results During hypoxia, PAPs, pulmonary ACE activity, HP increased significantly and SMC changed into secretive phenotype.Treatment with cilazapril, an ACE inhibitor, decreased ACE activity along with reversal of PAPs, HP and SMC phenotype. Conclusions Pulmonary ACE participated in the modulation of changes of SMC phenotype and collagen metabolism during hypoxic PAH.