• Bernd W Böttiger, Johann Motsch, Volker Braun, Eike Martin, and Michael Kirschfink.
• Department of Anesthesiology, University of Heidelberg, Germany. bernd_boettiger@med.uni-heidelberg.de
• Crit. Care Med. 2002 Nov 1;30(11):2473-80.

ObjectiveAnimal studies have demonstrated that reperfusion disorders occurring after cardiac arrest affect outcome. Reperfusion injury can be caused by activation of complement, polymorphonuclear leukocytes (PMN), and PMN-endothelial interaction. We studied different specific markers of these processes during and after cardiopulmonary resuscitation in humans.DesignProspective clinical trial.SettingUniversity hospital.PatientsA total of 55 patients who underwent out-of-hospital cardiopulmonary resuscitation for nontraumatic causes.InterventionsBlood samples were drawn immediately, 15 mins, and 30 mins after initiation of cardiopulmonary resuscitation. In the case of restoration of spontaneous circulation, additional blood samples were taken at serial time points until 7 days after cardiac arrest.Measurements And Main ResultsA marked activation of complement and PMN was found in all patients investigated. Serum concentrations of specific activation markers of the complement system, anaphylatoxin C3a and the soluble membrane attack complex SC5b-9, and PMN elastase were increased during cardiopulmonary resuscitation and for ConclusionsOur data clearly demonstrate a marked activation of complement and PMN and an increased PMN-endothelial interaction during cardiopulmonary resuscitation and early reperfusion after cardiac arrest in humans. These changes are known to induce reperfusion disorders and tissue injury and point to new therapeutic options to improve outcome after cardiac arrest.

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