Cardiopulmonary bypass (CPB) induces excessive production of endogenous proinflammatory mediators such as cytokines and elastase, which are responsible for the subsequent development of systemic inflammatory response syndrome (SIRS). In this study, we investigated the protective effect of rolipram against SIRS after CPB. Rats were divided into three groups (n = 5 in each): control (C), rolipram (R), and sham (S). Rats in groups C and R underwent CPB for 60 min followed by 60 min of observation, while those in group S were observed for 120 min without CPB. In group R, 40 microg/kg/min of rolipram was intravenously administered throughout the experiment. CD11b expression on neutrophils was analyzed using flow cytometry. Serum concentrations of tissue necrosis factor alpha (TNF-alpha), interleukin 1beta (IL-1beta), macrophage inflammatory protein 2 (MIP-2), and elastase were also determined. CD11b expression at the end of the experiment was unchanged from the initial value in group R, whereas that in group C increased to almost double, and that in group S also showed a slight increase (P < 0.01). Serum TNF-alpha levels in groups R and S were lower than those observed in group C (P < 0.05). Serum IL-1beta and MIP-2 levels in groups C and R tended to be higher than those in group S, although the difference was not statistically significant. Regarding elastase, group R showed a significantly lower value than group C and a higher value than group S (P < 0.05). Phosphodiesterase type 4 inhibition seems to suppress CPB-induced SIRS through the regulation of proinflammatory mediators in this rat model.