Out-of-hospital cardiac arrest increases soluble vascular endothelial adhesion molecules and neutrophil elastase associated with endothelial injury

• Published in: Intensive care medicine 2000-01, Vol.26 (1), p.38-44
• Main Authors: GANDO, S, NANZAKI, S, MORIMOTO, Y, KOBAYASHI, S, KEMMOTSU, O
• Format: Article
• Language: English
• Subjects: Anesthesia. Intensive care medicine. Transfusions. Cell therapy and gene therapy; Biological and medical sciences; Blood pressure; Cardiac arrest; Cardiopulmonary Resuscitation; Catheters; Cell adhesion & migration; CPR; E-Selectin - blood; Emergency and intensive cardiocirculatory care. Cardiogenic shock. Coronary intensive care; Emergency medical care; Emergency Medical Services; Emergency services; Endothelium; Female; Heart Arrest - blood; Heart Arrest - enzymology; Heart Arrest - mortality; Heart Arrest - therapy; Humans; Intensive care; Intensive care medicine; Intercellular Adhesion Molecule-1 - blood; Ischemia; Leukocyte Elastase - blood; Male; Medical sciences; Middle Aged; Neutrophil Activation; Neutrophils; Prospective Studies; Thrombomodulin - blood; Vascular Cell Adhesion Molecule-1 - blood
• ISSN: 0342-4642; 1432-1238
• DOI: 10.1007/s001340050009

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. Prospective, cohort study. General intensive care unit of a tertiary care center. 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. 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. 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.