过氧化氢诱导肺微血管内皮损伤的实验研究

目的　探讨H2 O2 诱导培养肺微血管内皮细胞损伤的机制。方法　观察H2 O2 对大鼠肺微血管内皮细胞 (RP MVEC)的形态、单层通透性、F 肌动蛋白和 β AR的影响。结果　H2 O2 浓度大于 1mmol·L-1作用 48h内观察到细胞脱落和破裂。 10mmol·L-1H2 O2 90min内可使RPMVEC单层通透性增高、F 肌动蛋白发生明显解聚和 β AR显著下调 ;FOR、山莨菪碱和CTX可抑制上述变化。结论　H2 O2引起的RPMVEC脱落与破裂呈浓度和时间依赖性。H2 O2引起RPMVEC单层通透性增高的机制与F 肌动蛋白解聚密切相关 ;β AR参与内皮通透性调节。FOR、山莨菪碱和CTX对H2 O2 引起RPMVEC单层通透性增高有一定的保护作用。

Experimental research on peroxide hydrogen induced injury of pulmonary microvascular endothelial cells

AIM To investigate the mechanism of peroxide hydrogen(H 2O 2) induced injury on the cultured pulmonary microvascular endothelial cell METHODS The effects of H 2O 2 on morphology, monolayer permeability, F actin distribution and β adrenoceptor(β AR) of rat pulmonary microvascular endothelial cell(RPMVEC) were observed RESULTS H 2O 2 in the concentration larger than 1 mmol·L -1 induced detatchment and rupture of RPMVEC within 48 h 10 mg·L -1 of H 2O 2 induced the increased permeability of RPMVEC monolayer, depolymerization of F actin and down regulation of β AR within 90 min Formoterol(FOR), anisodamine and cholera toxin(CTX) inhibited the effects of H 2O 2 CONCLUSION The detatchment and rupture of RPMVEC induced with H 2O 2 depends on the exposed concentration and time The increased permeability of RPMVEC monolayer induced with H 2O 2 is densely correlated with the depolymerization of F actin β AR participates in regulation of endothelial permeability FOR, anisodamine and CTX exert protective action to H 2O 2 induced RPMVEC injury