Objective:To investigate the relationship between cytokines and the inflamm
atory responses in patients with out-of-hospital cardiac arrest, we examine
d the changes of cytokines as well as alterations in the markers of neutrop
hil activation, platelet and endothelial activation, and endothelial injury
.
Design: Prospective. cohort study.
Setting: General intensive cart: unit of a tertiary care center.
Patients and participants: 26 out-of-hospital cardiac arrest patients were
classified into two groups: these who achieved return of spontaneous circul
ation (ROSC) (n = 10) and those with no ROSC (n = 16). Eight normal healthy
volunteers served as control subjects.
Measurements and results: Serial levels of soluble L-selectin (sL-selectin)
, soluble P-selectin (sP-selectin), neutrophil elastase, and soluble thromb
omodulin were measured during and after cardiopulmonary resuscitation (CPR)
. Serial levels of tumor necrosis factor alpha (TNF alpha) and interleukin-
1 beta (IL-1 beta) 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 these in control subjects from the time of
arrival at the emergency department to 24 h after admission, sL-selectin le
vels in the two groups were markedly lower compared to these in control sub
jects at all sampling points. In patients with ROSC, cardiac arrest and CPR
led to an increase in the levels of neutrophil elastase and soluble thromb
omodulin 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 duri
ng CPR.
Conclusions: Out-of-hospital cardiac arrest and CPR induces platelet, neutr
ophil. and endothelial activation and is associated with endothelial injury
, Inflammatory cytokines may not have an important role in human whole-body
ischemia-reperfusion injury.