Olprinone decreases elevated concentrations of cytokine-induced neutrophil chemoattractant-1 in septic rats

Abstract

The diaphragm is one of the organs directly affected by abdominal sepsis. Evidence suggests that sepsis induces diaphragmatic fatigability and that activated neutrophils play a crucial role in the development of diaphragmatic fatigability. In the present study, we investigated whether olprinone, a phosphodiesterase inhibitor, influenced the kinetics of cytokine-induced neutrophil chemoattractant-1 (CINC-1) in the diaphragm under abdominal septic conditions. Male Wistar rats were randomly assigned to a sham group, a cecal ligation and perforation group, and a phosphodiesterase inhibitor-pretreated group. To measure serial changes in CINC-1 concentrations, the right hemidiaphragm was removed at 4, 8, and 16 h after the surgical procedure in each group. In the cecal ligation and perforation group, CINC-1 concentrations in the diaphragm were significantly elevated compared with those in the sham group at both 4 and 8 h after the cecal ligation and perforation procedure. In the phosphodiesterase inhibitor-pretreated group, olprinone significantly attenuated the elevated CINC-1 concentrations at both 4 and 8 h after the surgical procedure. However, we observed no statistically significant differences in CINC-1 concentrations between the cecal ligation and perforation group and the phosphodiesterase inhibitor-pretreated groups at 16 h after the surgical procedure. Olprinone decreases elevated CINC-1 concentration in the diaphragm under septic conditions. This suggests that olprinone may inhibit neutrophil recruitment to the diaphragm.