title: Significant [C3a] increase in free flaps after prolonged ischemia.
abstract: BACKGROUND
  Free tissue transfer (FTT) represents a clinical model to measure ischemia-reperfusion injury (IRI). This study was conducted to detect substances relevant for IRI after FTT.
  
  
  METHODS
  Eighteen patients underwent lower leg reconstruction with free myocutaneous latissimus dorsi muscles and were monitored clinically and by microdialysis technique. Patients were retrospectively classified as group A (n = 12) (no prolonged IRI) or group B (n = 6) (prolonged IRI). One catheter was placed into the flap and one into the reference tissue. Samples were collected during ischemia and in 90 min steps after reperfusion. Biochemical substances (glucose, pyruvate, lactate, and glycerol) and immunological substances (interleukin 8 [IL-8], complement 3a [C3a], and regulated on activation normal T cell expressed and secreted [RANTES]) were then analyzed.
  
  
  RESULTS
  All free myocutaneous latissimus dorsi flaps healed primarily. Minor complications included revisions of the microvascular anastomoses due to hematoma or thrombus formation and increased total flap ischemia time in group B significantly when compared to group A (P < 0.001). No significant differences of biochemical substance concentrations were detected during reperfusion in target and control tissue of both groups. IL-8 and C3a were at detectable levels, whereas the results for RANTES were inconsistent. Either for group A and group B, we found higher concentrations of C3a in target tissue compared with control tissue. Furthermore, during the first 90 min of reperfusion, we found a highly significant increase of C3a (P < 0.001) in the target tissue of patients with increased ischemia time.
  
  
  CONCLUSIONS
  Given our results, C3a is a highly sensitive early indicator of ischemia-reperfusion damage. Our results give further insight into development of IRI after complicated FTT.
authors.affiliation: Department of Plastic and Hand Surgery, University of Luebeck, Luebeck, Germany.
authors.forename: Anne
authors.initials: A
authors.lastname: Brueggemann
authors.forename: Ariel
authors.initials: A
authors.lastname: Noltze
authors.forename: Thomas
authors.initials: T
authors.lastname: Lange
authors.forename: Michael
authors.initials: M
authors.lastname: Kaun
authors.forename: Jan
authors.initials: J
authors.lastname: Gliemroth
authors.forename: Siegfried
authors.initials: S
authors.lastname: Goerg
authors.forename: Ludger
authors.initials: L
authors.lastname: Bahlmann
authors.forename: Stephan
authors.initials: S
authors.lastname: Klaus
authors.forename: Frank
authors.initials: F
authors.lastname: Siemers
authors.forename: Peter
authors.initials: P
authors.lastname: Mailaender
authors.forename: Hans-Guenther
authors.initials: HG
authors.lastname: Machens
mesh_terms: D000293:Adolescent; D000328:Adult; D018946:Chemokine CCL5 / Q000378:metabolism; D015926:Complement C3a / Q000378:metabolism*; D045604:Extracellular Fluid / Q000378:metabolism*; D005260:Female; D005947:Glucose / Q000378:metabolism; D005990:Glycerol / Q000378:metabolism; D006801:Humans; D020382:Interleukin-18 / Q000378:metabolism; D007511:Ischemia / Q000378:metabolism*; D019344:Lactic Acid / Q000378:metabolism; D008297:Male; D017551:Microdialysis; D008875:Middle Aged; D018482:Muscle, Skeletal / Q000098:blood supply* / Q000378:metabolism / Q000637:transplantation; D011446:Prospective Studies; D019289:Pyruvic Acid / Q000378:metabolism
chemical_list: D018946:Chemokine CCL5; D020382:Interleukin-18; D019344:Lactic Acid; D015926:Complement C3a; D019289:Pyruvic Acid; D005947:Glucose; D005990:Glycerol