摘要
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.
出处
《中华结核和呼吸杂志》
CSCD
北大核心
1997年第4期215-217,共3页
Chinese Journal of Tuberculosis and Respiratory Diseases