title: Heparin-coated circuits reduce the formation of TNF alpha during cardiopulmonary bypass.
abstract: BACKGROUND
  Cardiopulmonary bypass (CPB) causes a systemic inflammatory response. TNF alpha, which is a major inflammatory mediator, has been found in the circulation during and after CPB. Although previous studies have shown that heparin coating of the extracorporeal circuits reduces complement and granulocyte activation, and the inflammatory response, the possible effect of heparin coating on TNF alpha formation and the inflammatory response has not been fully investigated.
  
  
  METHODS
  Eighteen patients scheduled for coronary artery bypass grafting were divided randomly into two groups. One group of patients had extracorporeal perfusion using heparin coated circuits (HC group, n = 9). The other group had extra-corporeal perfusion using an identical circuit that was not coated (UC group, n = 9). Blood samples were drawn before, during, and after CPB for measurement of plasma TNF alpha, plasma IL-8, neutrophil count, and neutrophil elastase.
  
  
  RESULTS
  Plasma levels of TNF alpha increased during CPB in the UC group but not in the HC group. Plasma concentrations of IL-8 increased similarly during and after CPB in both groups. Coating the circuits with heparin did not affect the levels of IL-8. In both groups, the neutrophil count increased after the release of the aortic cross clamp and remained elevated for three days. In the HC group, however, the increase of neutrophil count was significantly lower compared with the UC group. Plasma concentrations of neutrophil elastase were significantly increased during and after CPB in both groups. However, the levels of elastase were significantly lower at certain time points in the HC group.
  
  
  CONCLUSIONS
  From these observations, we conclude that heparin coating of the extracorporeal circuits reduces the TNF alpha formation during CPB, which may reduce neutrophil activation.
authors.affiliation: Kanagawa Prefectural Cardiorespiratory Center, Department of Anesthesiology, Yokohama City University School of Medicine, Japan.
authors.forename: H
authors.initials: H
authors.lastname: Yamada
authors.forename: I
authors.initials: I
authors.lastname: Kudoh
authors.forename: Y
authors.initials: Y
authors.lastname: Hirose
authors.forename: M
authors.initials: M
authors.lastname: Toyoshima
authors.forename: H
authors.initials: H
authors.lastname: Abe
authors.forename: K
authors.initials: K
authors.lastname: Kurahashi
mesh_terms: D000925:Anticoagulants / Q000008:administration & dosage / Q000627:therapeutic use*; D002315:Cardiopulmonary Bypass / Q000295:instrumentation*; D001026:Coronary Artery Bypass; D017558:Elective Surgical Procedures; D004867:Equipment Design; D006493:Heparin / Q000008:administration & dosage / Q000627:therapeutic use*; D006801:Humans; D007249:Inflammation; D018836:Inflammation Mediators / Q000032:analysis / Q000378:metabolism*; D016209:Interleukin-8 / Q000097:blood; D007958:Leukocyte Count / Q000187:drug effects; D019272:Leukocyte Elastase; D008875:Middle Aged; D009504:Neutrophils / Q000187:drug effects; D010196:Pancreatic Elastase / Q000097:blood; D013499:Surface Properties; D014409:Tumor Necrosis Factor-alpha / Q000032:analysis / Q000096:biosynthesis*
chemical_list: D000925:Anticoagulants; D018836:Inflammation Mediators; D016209:Interleukin-8; D014409:Tumor Necrosis Factor-alpha; D006493:Heparin; D010196:Pancreatic Elastase; D019272:Leukocyte Elastase