title: Comparison of blood activation in the wound, active vent, and cardiopulmonary bypass circuit.
abstract: BACKGROUND
  During cardiopulmonary bypass, aspirated blood exhibits strong activation features, but the triggering event remains unclear. Contact of blood with the pericardial cavity and surgical wound has been advocated as the main trigger, but suction forces are also considered as a possible contributor. We thus designed a study to identify the possible causes involved in this activation.
  
  
  METHODS
  In 10 patients, we analyzed hemostasis activation markers and inflammatory mediators in blood collected in the pericardial cavity and in blood actively aspirated from the left ventricle without any contact with the pericardial cavity. In addition, the same variables were determined in blood sampled in the cardiopulmonary bypass circuit.
  
  
  RESULTS
  Markers of tissue factor pathway activation and of thrombin generation, microparticles, free hemoglobin, interleukin 6, and tumor necrosis factor-alpha were significantly increased in pericardial samples as compared with the left ventricle and cardiopulmonary bypass circuit samples. All measured variables were similar between left ventricle and cardiopulmonary bypass samples, except free hemoglobin, interleukin 6, and microparticle levels, which were significantly higher in the left ventricle.
  
  
  CONCLUSIONS
  Blood contact with the pericardial cavity induces strong hemolysis, inflammatory mediator release, and coagulation activation, driven by tissue factor pathway activation. By contrast, suction forces applied to left ventricular blood poorly contribute to blood trauma and activation. Comparison of pericardial and left ventricular blood shows that contact with the pericardial cavity, and not suction forces, is the leading cause of blood activation. The specific trigger for blood trauma and activation present in the pericardial cavity remains to be identified.
authors.affiliation: Centre Hospitalier Régional Universitaire de Lille, Clinique de Chirurgie Cardiovasculaire, Lille, France. o-fabre@chru-lille.fr
authors.forename: Olivier
authors.initials: O
authors.lastname: Fabre
authors.forename: André
authors.initials: A
authors.lastname: Vincentelli
authors.forename: Delphine
authors.initials: D
authors.lastname: Corseaux
authors.forename: Francis
authors.initials: F
authors.lastname: Juthier
authors.forename: Sophie
authors.initials: S
authors.lastname: Susen
authors.forename: Anne
authors.initials: A
authors.lastname: Bauters
authors.forename: Eric
authors.initials: E
authors.lastname: Van Belle
authors.forename: Frédéric
authors.initials: F
authors.lastname: Mouquet
authors.forename: Thierry
authors.initials: T
authors.lastname: Le Tourneau
authors.forename: Christophe
authors.initials: C
authors.lastname: Decoene
authors.forename: Francis
authors.initials: F
authors.lastname: Crépin
authors.forename: Alain
authors.initials: A
authors.lastname: Prat
authors.forename: Brigitte
authors.initials: B
authors.lastname: Jude
mesh_terms: D000368:Aged; D000787:Angina Pectoris / Q000601:surgery; D001777:Blood Coagulation / Q000502:physiology*; D002315:Cardiopulmonary Bypass / Q000379:methods; D001026:Coronary Artery Bypass; D005260:Female; D005434:Flow Cytometry; D006324:Heart Arrest, Induced; D006801:Humans; D018836:Inflammation Mediators; D008297:Male; D008875:Middle Aged; D010496:Pericardium / Q000502:physiology*; D015539:Platelet Activation / Q000502:physiology; D013925:Thromboplastin / Q000032:analysis / Q000502:physiology*
chemical_list: D018836:Inflammation Mediators; D013925:Thromboplastin