血管紧张素Ⅱ及其受体拮抗剂对大鼠肺微血管内皮炎性损伤效应的影响

目的 探讨血管紧张素Ⅱ(Ang Ⅱ)及其受体对大鼠肺微血管内皮细胞(RPMVECs)单层通透性的影响。方法 在体外培养Wistar大鼠RPMVECs基础上,使用微型针头式滤器分别检测不同浓度脂多糖(LPS)作用不同时间前后RPMVECs单层滤过系数(Kf)的变化,AngⅡ对LPS致内皮通透性损伤作用的影响,以及AngⅡ的I型受体(AT1-R)拮抗剂[Sar1,Ile8]-AngⅡ的干预作用。结果 与正常对照组相比,LPS可致RPMVECs Kf明显升高;AngⅡ可显著恶化LPS致RPMVECs Kf升高的效用,而AT1-R拮抗剂(Sar1,Ile8]-AngⅡ干预后可明显抑制上述变化。结论 AngⅡ可显著恶化LPS对大鼠肺微血管通透性的炎性致伤作用,而AT1-R拮抗剂对炎性介质致大鼠肺微血管通透性损伤有明显的保护作用。

Inflammatory injurious effect of angiotensin Ⅱ on pulmonary microvascular endothelium in rat

OBJECTIVE: To investigate the effects of angiotensin II (AngII) and its receptors on monolayer permeability of pulmonary microvascular endothelial cells in rat. METHODS: The following examinations were done on cultured rat pulmonary microvascular endothelial cells (RPMVECs). 1. Micro-infiltrator was used to assay the variations of lipopolysaccharide (LPS)-induced increased RPMVECs monolayer permeability coefficient (Kf) in different periods. 2. Effect of angiotensin II on LPS-induced permeability injury to the endothelium, and preventive effects of angiotensin II type 1 receptor antagonist (Sar1, Ile8)-Ang II. RESULTS: LPS increased RPMVECs monolayer permeability compared with normal control, and AngII exacerbated LPS-induced RPMVECs monolayer permeability significantly. This synergistic effect was significantly prevented by the addition of (Sar1, Ile8 )-Ang II. CONCLUSION: AngII and LPS have synergistic injurious effects to the pulmonary microvascular endothelium in rat, and AngII exacerbates increase in LPS-induced RPMVECs monolayer permeability. This synergistic effect is significantly prevented by the addition of (Sar1, Ile8)-Ang II.