Activated cytokine production in patients with accidental hypothermia

Aibiki, Mayuki; Maekawa, Soichi; Nishiyama, Takashi; Seki, Keisuke; Yokono, Satoshi

doi:10.1016/s0300-9572(99)00052-0

Cited by 41 publications

(19 citation statements)

References 14 publications

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“…4 A possible mechanism for no effects on cytokines responses in post cardiac arrest patients undergoing hypothermia is that in the TTM trials, there might not be a strict control of hemodynamics ensuring the peripheral circulation, as done in our institution. 2,3 We found that in patients with accidental hypothermia, IL-6 and IL-8 increased remarkably, 5 which is supported by a paper demonstrating the relationship between cytokines and the depth of accidental hypothermia. 6 So, these papers clearly describe that hypothermia itself should be the cause of severe physiological stress to the human body.…”

Section: Sirsupporting

confidence: 63%

Can therapeutic hypothermia of 33°C itself not modulate inflammatory response after out-of-hospital cardiac arrest?

et al. 2015

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Section: Sirsupporting

confidence: 63%

Can therapeutic hypothermia of 33°C itself not modulate inflammatory response after out-of-hospital cardiac arrest?

et al. 2015

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“…However, in vivo concentrations of critical neutrophil activators such as TNF-␣ are highly temperature-dependent. Temperature dependence of cytokine release has been demonstrated for a variety of pro-and antiinflammatory cytokines in vivo (22)(23)(24). In vitro experiments with monocytes and macrophages as major generators of cytokines show that cytokine production is clearly temperature-dependent, with decreased production in hypothermia and hyperthermia (25,26).…”

Section: Discussionmentioning

confidence: 99%

Mild Hyperthermia Down-Regulates Receptor-Dependent Neutrophil Function

Fröhlich¹,

Wittmann²,

Rothe³

et al. 2004

Anesthesia & Analgesia

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Mild hypothermia impairs resistance to infection and, reportedly, impairs phagocytosis and oxidative killing of unopsonized bacteria. We evaluated various functions at 33 degrees-41 degrees C in neutrophils taken from volunteers. Adhesion on endothelial cells was determined using light microscopy. Adhesion molecule expression and receptors, phagocytosis, and release of reactive oxidants were assessed using flow cytometric assays. Adhesion protein CD11b expression on resting neutrophils was temperature-independent. However, up-regulation of CD11b with tumor necrosis factor (TNF)-alpha was increased by hypothermia and decreased with hyperthermia. Neutrophil adhesion to either resting or activated endothelial cells was not temperature-dependent. Bacterial uptake was inversely related to temperature, more so with Escherichia coli than Staphylococcus aureus. Temperature dependence of phagocytosis occurred only wi thopsonized bacteria. Hypothermia slightly increased N-formyl-L-methionyl-L-leucyl-phenylalanine receptors on neutrophils: hyperthermia decreased expression, especially with TNF-alpha. N-formyl-L-methionyl-L-leucyl-phenylalanine-induced H2O2 production was inversely related to temperature, especially in the presence of TNF-alpha. Conversely, phorbol-13-myristate-12-acetate, an activator of protein kinase C, induced an extreme and homogenous release of reactive oxidants that increased with temperature. In contrast to nonreceptor-dependent phagocytosis and oxidative killing, several crucial receptor-dependent neutrophil activities show temperature-dependent regulation, with hypothermia increasing function. The temperature dependence of neutrophil function is thus more complicated than previously appreciated.

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“…59 Interestingly, induced hypothermia has no effect on IL-6 levels in children, a finding that is in contrast to that observed in adult TBI patients in which IL-6 levels were found to decrease after therapeutic hypothermia. 60 …”

Section: Interleukin-6mentioning

confidence: 99%