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In order to explore the roles of tumor necrosis factor-α (TNF-α) and vascular endothelial growth factor (VEGF) in the pathogenesis of pulmonary emphysema, male Wistar rats were random-ized into group A<,1>, group A<,2.5> and group A<,4>, each with smoke exposure for 1 month, 2.5 months or 4 months, respectively. Group B<,1>, group B<,2.5> and group B<,4> were used as non smoking controls at corre-sponding time points. TNF-α in bronchoalveolar lavage fluid (BALF) and expression of VEGF in lung tissue was determined by ELISA or by SABC immunohistochemistry assay either. Lung slices were stained with hematoxylin and eosin (HE). Results showed that in animal with smoke exposure the mean linear interceptor (Lm), an index of pulmonary emphysema and the content of TNF-α in BALF increased gradually, on contrary, the expression of VEGF in lung tissue decreased (P<0.05).This phenomenon was not obvious in animals without smoke exposure. Lm was negatively correlated to the VEGF expression (γ=-0.81, P<0.01) and positively correlated to TNF-α concentration (γ=0.52, P<0.004), which implies that smoke exposure decreased the expression of VEGF and increased the expression of TNF-α. It is plausible to speculate that the imbalance of TNF-α and VEGF may play an important role in the pathogenesis of smoke-induced pulmonary emphysema.