• S Gando, S Nanzaki, Y Morimoto, S Kobayashi, and O Kemmotsu.
• Department of Anesthesiology and Intensive Care, Hokkaido University School of Medicine, N15 W7, Kita-ku, Sapporo, 060 Japan. sgando@med.hokudai.ac.jp
• Intensive Care Med. 2000 Jan 1;26(1):38-44.

ObjectivesTo 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.DesignProspective, cohort study.SettingGeneral intensive care unit of a tertiary care center.Patients And ParticipantsForty-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.Measurements And ResultsSerial 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.ConclusionsAs 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.

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