RESUMEN
Objective To establish the rat overlap syndrome (OS) model of intermittent hypoxia (IH) combined with pulmonary emphysema and to explore its connection with hepatic oxidative stress, inflammatory status in the live and coagu?lation profile. Methods Male Wistar rats (n=60) were randomly divided into four groups:control group (A), IH group (B), pulmonary emphysema group (C) and OS group (D). The rat model of pulmonary emphysema was established by exposing rats in smoke for 16 weeks. From the 13th week, pre-programmed intermittent hypoxia/re-oxygenation (IH/ROX) exposure was given in the meantime of smoke exposure in OS group. Liver tissues were sectioned or triturated for pathological scoring or for detecting expression levels of superoxide dismutase (SOD), catalase (CAT) and malondialdehyde (MDA) respectively. Se?rum levels of coagulant/anticoagulant factors such as antithrombin (AT), fibrinogen (FIB), von Willebrand factor(vWF) and FactorⅧ(FⅧ) were also evaluated using biochemistry analysis. Results The levels of pathological scores and coagulant factors(FIB, FⅧ:C and vWF:Ag)were significantly higher in group D than those in group A, B and C. The values of SOD, CAT and AT were significantly lower in group D than those in other three groups. Serum levels of FIB, vWF:Ag, FⅧ:C and AT:A correlated with SOD(r equal to-0.905、-0.941、-0.946 and 0.817 respective,P<0.01). Conclusion In rat overlap syndrome when IH combined with pulmonary emphysema, hepatic inflammation and coagulability present mutual promotion effect and produce a more significant liver-derivative inflammatory and prothrombotic status.