Marked activation of complement and leukocytes and an increase in the concentrations of soluble endothelial adhesion molecules during cardiopulmonary resuscitation and early reperfusion after cardiac arrest in humans.
OBJECTIVE
Animal 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.


METHODS
Prospective clinical trial.


METHODS
University hospital.


METHODS
A total of 55 patients who underwent out-of-hospital cardiopulmonary resuscitation for nontraumatic causes.


METHODS
Blood 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.


RESULTS
A 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 </=48 hrs after restoration of spontaneous circulation. Compared with controls at 30 mins after initiation of cardiac massage, concentrations of C3a, SC5b-9, and PMN elastase were increased in patients without and in those with restoration of spontaneous circulation. PMN elastase concentrations were significantly greater in patients without restoration of spontaneous circulation than in those who could be stabilized. In addition, the plasma concentrations of the soluble P-selectin were significantly increased between 15 mins and 24 hrs after the start of cardiopulmonary resuscitation. The concentrations of soluble intercellular adhesion molecule-1 were increased between 2 hrs and 72 hrs.


CONCLUSIONS
Our 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.
Böttiger
Bernd W
BW
Department of Anesthesiology, University of Heidelberg, Germany. bernd_boettiger@med.uni-heidelberg.de
Motsch
Johann
J
Braun
Volker
V
Martin
Eike
E
Kirschfink
Michael
M
D000368:Aged; D000706:Anaphylatoxins / Q000378:metabolism; D015415:Biomarkers; D016887:Cardiopulmonary Resuscitation; D016022:Case-Control Studies; D015815:Cell Adhesion Molecules / Q000378:metabolism*; D003167:Complement Activation; D015938:Complement Membrane Attack Complex / Q000378:metabolism; D005260:Female; D006323:Heart Arrest / Q000503:physiopathology* / Q000628:therapy; D006801:Humans; D018799:Intercellular Adhesion Molecule-1 / Q000097:blood; D019272:Leukocyte Elastase / Q000097:blood; D008297:Male; D008875:Middle Aged; D018375:Neutrophil Activation; D019007:P-Selectin / Q000097:blood; D011446:Prospective Studies; D015427:Reperfusion Injury / Q000276:immunology*; D018709:Statistics, Nonparametric
D000706:Anaphylatoxins; D015415:Biomarkers; D015815:Cell Adhesion Molecules; D015938:Complement Membrane Attack Complex; D019007:P-Selectin; D018799:Intercellular Adhesion Molecule-1; D019272:Leukocyte Elastase