title: Out-of-hospital cardiac arrest increases soluble vascular endothelial adhesion molecules and neutrophil elastase associated with endothelial injury.
abstract: OBJECTIVE
  To investigate the inflammatory responses in patients with out-of-hospital cardiac arrest, we examined the changes in markers of endothelial activation, neutrophil activation, and endothelial injury.
  
  
  METHODS
  Prospective, cohort study.
  
  
  METHODS
  General intensive care unit of a tertiary care center.
  
  
  METHODS
  Forty-four out-of-hospital cardiac arrest patients were classified into two groups, those who achieved return of spontaneous circulation (ROSC) (n = 23) and those without ROSC (n = 21). Eight normal healthy volunteers served as control subjects.
  
  
  RESULTS
  Serial levels of soluble intercellular adhesion molecule-1 (sICAM-1), soluble vascular cell adhesion molecule-1 (sVCAM-1), soluble E-selectin (sE-selectin) as markers of endothelial activation, neutrophil elastase as a marker of neutrophil activation, and soluble thrombomodulin as a marker of endothelial injury were measured during and after cardiopulmonary resuscitation (CPR). In patients with ROSC, cardiac arrest and CPR led to increases in the levels of three vascular endothelial adhesion molecules, neutrophil elastase, and soluble thrombomodulin that peaked 6 h or 24 h after arrival at the emergency department. In patients without ROSC, only neutrophil elastase showed moderate elevation during CPR. We could not find significant differences in all measured parameters between the two groups.
  
  
  CONCLUSIONS
  As evidence of inflammatory responses in whole-body ischemia and reperfusion, our study demonstrates neutrophil-endothelium interaction with signs of endothelial injury in patients with out-of-hospital cardiac arrest. These inflammatory changes may have an important role in post-resuscitation syndrome after human cardiac arrest.
authors.affiliation: Department of Anesthesiology and Intensive Care, Hokkaido University School of Medicine, N15 W7, Kita-ku, Sapporo, 060 Japan. sgando@med.hokudai.ac.jp
authors.forename: S
authors.initials: S
authors.lastname: Gando
authors.forename: S
authors.initials: S
authors.lastname: Nanzaki
authors.forename: Y
authors.initials: Y
authors.lastname: Morimoto
authors.forename: S
authors.initials: S
authors.lastname: Kobayashi
authors.forename: O
authors.initials: O
authors.lastname: Kemmotsu
mesh_terms: D016887:Cardiopulmonary Resuscitation; D019040:E-Selectin / Q000097:blood*; D004632:Emergency Medical Services; D005260:Female; D006323:Heart Arrest / Q000097:blood* / Q000201:enzymology / Q000401:mortality / Q000628:therapy; D006801:Humans; D018799:Intercellular Adhesion Molecule-1 / Q000097:blood*; D019272:Leukocyte Elastase / Q000097:blood*; D008297:Male; D008875:Middle Aged; D018375:Neutrophil Activation; D011446:Prospective Studies; D018180:Thrombomodulin / Q000097:blood*; D019010:Vascular Cell Adhesion Molecule-1 / Q000097:blood*
chemical_list: D019040:E-Selectin; D018180:Thrombomodulin; D019010:Vascular Cell Adhesion Molecule-1; D018799:Intercellular Adhesion Molecule-1; D019272:Leukocyte Elastase