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