• S Gando, S Nanzaki, Y Morimoto, S Kobayashi, and O Kemmotsu.
• Department of Anesthesiology and Intensive Care, Hokkaido University School of Medicine, Sapporo, Japan. sgando@med.hokudai.ac.jp
• Intensive Care Med. 1999 Jun 1;25(6):588-93.

ObjectiveTo investigate the relationship between cytokines and the inflammatory responses in patients with out-of-hospital cardiac arrest, we examined the changes of cytokines as well as alterations in the markers of neutrophil activation, platelet and endothelial activation, and endothelial injury.DesignProspective, cohort study.SettingGeneral intensive care unit of a tertiary care center.Patients And Participants26 out-of-hospital cardiac arrest patients were classified into two groups: those who achieved return of spontaneous circulation (ROSC) (n = 10) and those with no ROSC (n = 16). Eight normal healthy volunteers served as control subjects.Measurements And ResultsSerial levels of soluble L-selectin (sL-selectin), soluble P-selectin (sP-selectin), neutrophil elastase, and soluble thrombomodulin were measured during and after cardiopulmonary resuscitation (CPR). Serial levels of tumor necrosis factor alpha (TNFalpha) and interleukin-1beta (IL-1beta) were also measured. We could not find any elevations in either cytokine during the study period. In both groups, sP-selectin levels were significantly higher than those in control subjects from the time of arrival at the emergency department to 24 h after admission. sL-selectin levels in the two groups were markedly lower compared to those in control subjects at all sampling points. In patients with ROSC, cardiac arrest and CPR led to an increase in the levels of neutrophil elastase and soluble thrombomodulin that peaked 6 h or 24 h after arrival at the emergency department. No statistical differences in the levels of the two selectins, neutrophil elastase, and soluble thrombomodulin between the two groups were found during CPR.ConclusionsOut-of-hospital cardiac arrest and CPR induces platelet, neutrophil, and endothelial activation and is associated with endothelial injury. Inflammatory cytokines may not have an important role in human whole-body ischemia-reperfusion injury.

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