title: Tourniquet-induced systemic inflammatory response in extremity surgery.
abstract: BACKGROUND
  Tourniquet-induced reperfusion injury in animals produces significant systemic inflammatory effects. This study investigated whether a biologic response occurs in a clinically relevant model of tourniquet-induced reperfusion injury.
  
  
  METHODS
  Patients undergoing elective knee arthroscopy were prospectively randomized into controls (no tourniquet) and subjects (tourniquet-controlled). The effects of tourniquet-induced reperfusion on monocyte activation state, neutrophil activation state, and transendothelial migration (TEM) were studied. Changes in the cytokines implicated in reperfusion injury, tumor necrosis factor-alpha, interleukin (IL)-1beta, and IL-10 were also determined.
  
  
  RESULTS
  After 15 minutes of reperfusion, neutrophil and monocyte activation were significantly increased. Pretreatment of neutrophils with pooled subject (ischemia-primed) plasma significantly increased TEM. In contrast, TEM was not significantly altered by ischemia-primed plasma pretreatment of the endothelial monolayer. Significant elevation of tumor necrosis factor-alpha and IL-1beta were observed in subjects compared with controls after 15 minutes of reperfusion. There was no significant difference in serum IL-10 levels between the groups at all the time points studied.
  
  
  CONCLUSIONS
  These results indicate a transient neutrophil and monocyte activation after tourniquet-ischemia that translates into enhanced neutrophil transendothelial migration with potential for tissue injury.
authors.affiliation: Department of Academic Surgery, Cork University Hospital, Cork, Ireland.
authors.forename: A
authors.initials: A
authors.lastname: Wakai
authors.forename: J H
authors.initials: JH
authors.lastname: Wang
authors.forename: D C
authors.initials: DC
authors.lastname: Winter
authors.forename: J T
authors.initials: JT
authors.lastname: Street
authors.forename: R G
authors.initials: RG
authors.lastname: O'Sullivan
authors.forename: H P
authors.initials: HP
authors.lastname: Redmond
mesh_terms: D000328:Adult; D000704:Analysis of Variance; D019645:Arthroplasty, Replacement, Knee; D018845:CD11 Antigens / Q000097:blood; D002464:Cell Migration Inhibition; D002478:Cells, Cultured; D016207:Cytokines / Q000097:blood; D005260:Female; D006801:Humans; D018950:Lipopolysaccharide Receptors / Q000097:blood; D008297:Male; D009504:Neutrophils / Q000276:immunology; D011446:Prospective Studies; D015427:Reperfusion Injury / Q000097:blood / Q000150:complications*; D018746:Systemic Inflammatory Response Syndrome / Q000097:blood / Q000209:etiology*; D014111:Tourniquets / Q000009:adverse effects*
chemical_list: D018845:CD11 Antigens; D016207:Cytokines; D018950:Lipopolysaccharide Receptors