Successful cardiopulmonary resuscitation after cardiac arrest as a "sepsis-like" syndrome.
BACKGROUND
We investigated the immunoinflammatory profile of patients successfully resuscitated after cardiac arrest, representing a model of whole-body ischemia/reperfusion syndrome.


RESULTS
Plasma cytokine, endotoxin, and ex vivo cytokine production in whole-blood assays was assessed in 61, 35, and 11 patients, respectively. On admission, high levels of plasma interleukin (IL)-6, IL-8, IL-10, and soluble tumor necrosis factor (TNF) receptor type II could discriminate between survivors and nonsurvivors. Among nonsurvivors, the initial need for a vasopressor agent was associated with higher levels of IL-1 receptor antagonist, IL-10, and IL-6 on day 1. Plasma endotoxin was detected in 46% of the analyzed patients within the 2 first days. Endotoxin-induced TNF and IL-6 productions were dramatically impaired in these patients compared with healthy control subjects, whereas an unaltered production was observed with heat-killed Staphylococcus aureus. In contrast, IL-1 receptor antagonist productions were enhanced in these patients compared with healthy control subjects. The productions of T-cell-derived IL-10 and interferon-gamma were also impaired in these patients. Finally, using in vitro plasma exchange between healthy control subjects and patients, we demonstrated that the endotoxin-dependent hyporeactivity was an intrinsic property of patients' leukocytes and that an immunosuppressive activity was also present in their plasma.


CONCLUSIONS
Altogether, the high levels of circulating cytokines, the presence of endotoxin in plasma, and the dysregulated production of cytokines found in these patients recall the immunological profile found in patients with sepsis.
Adrie
Christophe
C
Medical ICU, Cochin Hospital, Paris, France. christophe.adrie@wanadoo.fr
Adib-Conquy
Minou
M
Laurent
Ivan
I
Monchi
Mehran
M
Vinsonneau
Christophe
C
Fitting
Catherine
C
Fraisse
François
F
Dinh-Xuan
A Tuan
AT
Carli
Pierre
P
Spaulding
Christian
C
Dhainaut
Jean-François
JF
Cavaillon
Jean-Marc
JM
D000368:Aged; D015703:Antigens, CD / Q000097:blood; D016887:Cardiopulmonary Resuscitation / Q000706:statistics & numerical data*; D016207:Cytokines / Q000097:blood; D004731:Endotoxins / Q000097:blood; D005260:Female; D015600:Glasgow Coma Scale; D006323:Heart Arrest / Q000150:complications / Q000503:physiopathology* / Q000628:therapy*; D006801:Humans; D053590:Interleukin 1 Receptor Antagonist Protein; D016753:Interleukin-10 / Q000097:blood; D015850:Interleukin-6 / Q000097:blood; D016209:Interleukin-8 / Q000097:blood; D007962:Leukocytes / Q000276:immunology; D008297:Male; D008875:Middle Aged; D010949:Plasma / Q000276:immunology; D011237:Predictive Value of Tests; D011446:Prospective Studies; D018124:Receptors, Tumor Necrosis Factor / Q000097:blood; D047889:Receptors, Tumor Necrosis Factor, Type II; D012016:Reference Values; D015427:Reperfusion Injury; D012795:Sialoglycoproteins / Q000097:blood; D015996:Survival Rate; D018746:Systemic Inflammatory Response Syndrome / Q000150:complications / Q000175:diagnosis / Q000503:physiopathology*; D016896:Treatment Outcome
D015703:Antigens, CD; D016207:Cytokines; D004731:Endotoxins; C507763:IL1RN protein, human; D053590:Interleukin 1 Receptor Antagonist Protein; D015850:Interleukin-6; D016209:Interleukin-8; D018124:Receptors, Tumor Necrosis Factor; D047889:Receptors, Tumor Necrosis Factor, Type II; D012795:Sialoglycoproteins; D016753:Interleukin-10