title: Release of inflammatory mediators in irradiated cell salvage blood and their biological consequences in human beings following transfusion.
abstract: OBJECTIVE
  Irradiation of intraoperative cell salvage blood has recently been used to inactivate tumour cells before retransfusion, during cancer surgery. No information is available about a potential inflammatory response of the recipient to the retransfusion of irradiated intraoperative cell salvage blood. This pilot study was conducted to investigate the possible release of the pro-inflammatory mediators, tumour necrosis factor-alpha (TNF-alpha), interleukin-1beta (IL-1beta), eotaxin and monocyte chemo-attractant protein-1 (MCP-1), in the serum of recipients by intraoperative retransfusion of irradiated intraoperative cell salvage blood.
  
  
  METHODS
  Nine patients undergoing gynaecological cancer surgery were included in this study. Intraoperative cell salvage blood was irradiated with 50 Gy and retransfused to the patient. Serum and intraoperative cell salvage blood concentrations of TNF-alpha, IL-1beta, eotaxin and MCP-1 were repeatedly analysed before and after retransfusion, respectively before and after irradiation.
  
  
  RESULTS
  Traces of mediators were detected in intraoperative cell salvage blood but no increase due to irradiation was observed. Following transfusion of intraoperative cell salvage blood, minute quantities (all < 30 pg mL(-1) of mediators were detected in the serum of patients. However, there was no significant upregulation compared to serum values before retransfusion.
  
  
  CONCLUSIONS
  These results provide evidence that retransfusion of irradiated intraoperative cell salvage blood might represent a blood-saving strategy in cancer surgery without an immunological inflammatory response as shown by a lack of upregulation of inflammatory mediators.
authors.affiliation: University Hospital, Institute of Anaesthesiology, Zurich, Switzerland. beatrice.beck@usz.ch
authors.forename: B
authors.initials: B
authors.lastname: Beck-Schimmer
authors.forename: B
authors.initials: B
authors.lastname: Romero
authors.forename: C
authors.initials: C
authors.lastname: Booy
authors.forename: H
authors.initials: H
authors.lastname: Joch
authors.forename: U
authors.initials: U
authors.lastname: Hallers
authors.forename: T
authors.initials: T
authors.lastname: Pasch
authors.forename: D R
authors.initials: DR
authors.lastname: Spahn
mesh_terms: D000368:Aged; D001793:Blood Preservation; D001804:Blood Transfusion, Autologous / Q000009:adverse effects* / Q000379:methods*; D054413:Chemokine CCL11; D018932:Chemokine CCL2 / Q000097:blood; D019742:Chemokines, CC / Q000097:blood; D042783:Endothelial Cells / Q000378:metabolism; D005260:Female; D013509:Gynecologic Surgical Procedures; D006801:Humans; D018836:Inflammation Mediators / Q000097:blood*; D018799:Intercellular Adhesion Molecule-1 / Q000096:biosynthesis; D007375:Interleukin-1 / Q000097:blood; D007958:Leukocyte Count; D008875:Middle Aged; D011827:Radiation; D013242:Sterilization; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism
chemical_list: C515456:CCL11 protein, human; D054413:Chemokine CCL11; D018932:Chemokine CCL2; D019742:Chemokines, CC; D018836:Inflammation Mediators; D007375:Interleukin-1; D014409:Tumor Necrosis Factor-alpha; D018799:Intercellular Adhesion Molecule-1