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ASAIO CARDIAC ABSTRACT

PHOSPHODIESTERASE TYPE 4 INHIBITOR ATTENUATES SYSTEMIC INFLAMMATORY RESPONSE INDUCED BY CARDIOPULMONARY BYPASS IN A RAT MODEL

Hamamoto, M.1; Suga, M.1; Takahashi, Y.1; Sato, Y.2; Inamori, S.1; Yagihara, T.1; Nakatani, T.1; Kitamura, S.1

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Activated neutrophils during cardiopulmonary bypass (CPB) play a key role for the induction of systemic inflammatory responses syndrome (SIRS), which causes vital organ failure. A phosphodiesterase type 4 inhibitor, rolipram, blocks neutrophil activation by the inhibition of CAMP decomposition. In this study, we verified the protective effect of rolipram on CPB-induced SIRS in a rat model. Sprague Dawley rats were divided into three groups (n = 5 for each): Control (C), Rolipram (R) and Sham (5). Rats in C and R underwent CPB at the flow rate of 60 ml/kg/min for 60 minutes followed by another 60-minutes observation. Rats in S were sustained for 120 minutes without CPB after cannulation. In R, rolipram (40μg/kg/min) was intravenously administered during the experiment. The expression of CDllb on neutrophils, serum level of TNF-α, IL-lβ, IL-6, MIP-2 and neutrophil elastase were evaluated. CD11b expression after CPB remained the same in R and mildly increased in s, although that in C reached more than the double and higher than the others (R: 102 ± 26, S: 153 ± 66, C: 235 ± 53% of pre-CPB value, p<0.05). Serum TNF-α levels in R and S were lower than that in C (R: 4600 ± 4400, S: 4200 ± 3900, C: 1 5500 ± 6100 pg/ml, p<0.05). In contrast, no significant differences were observed in IL-lβ, IL-6, and MIP-2 levels among the groups. As for serum elastase, R showed lower value than C (p<0.05). These results suggest that rolipram attenuates SIRS induced by CPB via the inhibition of neutrophil activation in this rat model.

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