Soluble selectins and the systemic inflammatory response syndrome after successful cardiopulmonary resuscitation

Geppert, Alexander; Zorn, Gerlinde; Karth, Georg Delle; Haumer, Markus; Gwechenberger, Marianne; Koller-Strametz, J; Heinz, Gottfried; Huber, Kurt; Siostrzonek, Peter

doi:10.1097/00003246-200007000-00030

Cited by 77 publications

(38 citation statements)

References 26 publications

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“…112 Soluble intercellular adhesion molecule-1, soluble vascular cell adhesion molecule-1, and P-and E-selectins are increased during and after CPR, which suggests leukocyte activation or endothelial injury. 114,115 Interestingly, hyporesponsiveness of circulating leukocytes, as assessed ex vivo, has been studied extensively in patients with sepsis and is termed "endotoxin tolerance." Endotoxin tolerance after cardiac arrest may protect against an overwhelming proinflammatory process, but it may induce immunosuppression with an increased risk of nosocomial infection.…”

Section: Systemic Ischemia/reperfusion Responsementioning

confidence: 99%

Post–Cardiac Arrest Syndrome

Neumar¹,

Nolan²,

Adrie³

et al. 2008

Circulation

1,231

398

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Section: Systemic Ischemia/reperfusion Responsementioning

confidence: 99%

Post–Cardiac Arrest Syndrome

Neumar¹,

Nolan²,

Adrie³

et al. 2008

Circulation

1,231

398

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“…Many studies have demonstrated that the body experiences ischemia-reperfusion injury (IRI) after CPR due to cardiac arrest. Under this condition, the endothelial system and inflammatory cascade were activated resulting in systemic inflammatory response syndrome; further aggravation of this condition may cause multiple organ failure, which is a major cause of poor prognosis [2][3][4]. It is reasonable to speculate that promoting the regression of inflammation is important to advanced life support following CPR.…”

Section: Introductionmentioning

confidence: 99%

Effect of Lipoxin A4 on Myocardial Ischemia Reperfusion Injury Following Cardiac Arrest in a Rabbit Model

Chen

Huang

et al. 2012

Inflammation

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In the present study, we investigated the effect of lipoxin A4 on myocardial ischemia-reperfusion injury (IRI) following cardiac arrest (CA) in a rabbit model. Lipoxin A4 is a metabolite of arachidonic acid in the eicosanoid, it is called "brake signal" for its anti-inflammatory activity. Some inflammatory factors (IL-1β, IL-6, TNF-α, and IL-10), NF-κB p65, infarct ratios, apoptotic index, cardiac troponin I (cTnI), hemodynamic and myocardial structures were measured or observed in different groups. Lipoxin A4 inhibits the expression of IL-1β, IL-6, and TNF-α, the values of the infarct ratios, apoptotic index, the level of serum cTnI and NF-κB p65. Meanwhile, it improves the expression of IL-10, hemodynamic, myocardial structure, and function. These indicate that lipoxin A4 mitigates postresuscitation myocardial IRI in which anti-inflammation and suppression of NF-κB activation may play an important role.

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“…1 During and after cardiopulmonary resuscitation, activation of blood coagulation, 2,3 platelet activation with formation of thromboxane A 2 , 4 and an alteration of soluble E-selectin and P-selectin 5 have been described. More challenging are the pathophysiological disturbances, described as "postresuscitation" disease 6 (observed after the return to spontaneous circulation), such as hypovolemic shock, cardiogenic shock, and vasodilatory shock.…”

mentioning

confidence: 99%

“…We hypothesized that postresuscitation disease may be related to an early systemic inflammatory response, leading to an exacerbation of the inflammatory balance, 5,7 and may possibly be associated with an "endotoxin tolerance," as observed in severe sepsis. 8 In the present study, we investigated (1) the kinetics of plasma cytokines after a successfully resuscitated cardiac arrest, (2) the plasma endotoxin levels, and (3) the occurrence of dysregulation of the immune response assessed by ex vivo cytokine production by blood leukocytes.…”

mentioning

confidence: 99%

Successful Cardiopulmonary Resuscitation After Cardiac Arrest as a “Sepsis-Like” Syndrome

et al. 2002

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Background-We investigated the immunoinflammatory profile of patients successfully resuscitated after cardiac arrest, representing a model of whole-body ischemia/reperfusion syndrome. Methods and 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-␥ 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. (Circulation. 2002;106:562-568.)

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Soluble selectins and the systemic inflammatory response syndrome after successful cardiopulmonary resuscitation

Abstract: SIRS is an unspecific finding after CPR with only minor impact on outcome. Determination of sP- and sE-selectin early after CPR might help to identify patients at a high risk for sepsis or for an adverse outcome, respectively.

Cited by 77 publications

References 26 publications

Post–Cardiac Arrest Syndrome

Post–Cardiac Arrest Syndrome

Effect of Lipoxin A4 on Myocardial Ischemia Reperfusion Injury Following Cardiac Arrest in a Rabbit Model

Successful Cardiopulmonary Resuscitation After Cardiac Arrest as a “Sepsis-Like” Syndrome

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