title: Olprinone decreases elevated concentrations of cytokine-induced neutrophil chemoattractant-1 in septic rats.
abstract: OBJECTIVE
  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.
  
  
  METHODS
  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.
  
  
  RESULTS
  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.
  
  
  CONCLUSIONS
  Olprinone decreases elevated CINC-1 concentration in the diaphragm under septic conditions. This suggests that olprinone may inhibit neutrophil recruitment to the diaphragm.
authors.affiliation: Department of Anesthesiology, Faculty of Medicine, Oita University, Yufu, Oita, Japan.
authors.forename: Hiroshi
authors.initials: H
authors.lastname: Miyakawa
authors.forename: Shinichiro
authors.initials: S
authors.lastname: Kira
authors.forename: Kentaro
authors.initials: K
authors.lastname: Okuda
authors.forename: Naozumi
authors.initials: N
authors.lastname: Takeshima
authors.forename: Masakazu
authors.initials: M
authors.lastname: Mori
authors.forename: Takayuki
authors.initials: T
authors.lastname: Noguchi
mesh_terms: D000818:Animals; D054360:Chemokine CXCL1 / Q000187:drug effects* / Q000378:metabolism; D003964:Diaphragm / Q000378:metabolism*; D007093:Imidazoles / Q000494:pharmacology*; D007274:Injections, Intraperitoneal; D008297:Male; D018375:Neutrophil Activation / Q000187:drug effects; D010726:Phosphodiesterase Inhibitors / Q000494:pharmacology*; D011728:Pyridones / Q000494:pharmacology*; D011897:Random Allocation; D051381:Rats; D017208:Rats, Wistar; D018805:Sepsis / Q000188:drug therapy / Q000378:metabolism*; D016896:Treatment Outcome
chemical_list: D054360:Chemokine CXCL1; C513297:Cxcl1 protein, rat; D007093:Imidazoles; D010726:Phosphodiesterase Inhibitors; D011728:Pyridones; C059498:olprinone