Prior Ethanol Injection Promotes Brain Edema after Traumatic Brain Injury

Katada, Ryuichi; Nishitani, Yoko; Okazaki, Shunichiro; Houkin, Kiyohiro; Matsumoto, Hiroshi

doi:10.1089/neu.2008.0552

Cited by 23 publications

(18 citation statements)

References 41 publications

(36 reference statements)

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“…In addition, ethanol has been shown to be associated with respiratory depression, apnoea and hypoxia [3][4][5], which may contribute to secondary insults following TBI. Raised intracranial pressures and acidaemia have also been reported as potential adverse effects of ethanol exposure [6][7][8].…”

Section: Introductionmentioning

confidence: 99%

Ethanol and isolated traumatic brain injury

Brennan

Bernard

Cameron

et al. 2015

Journal of Clinical Neuroscience

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Section: Introductionmentioning

confidence: 99%

Ethanol and isolated traumatic brain injury

Brennan

Bernard

Cameron

et al. 2015

Journal of Clinical Neuroscience

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“…9 Activation of NF-jB has likewise been documented in the brain after TBI. [10][11][12][13][14] The precise role of this transcription factor in the development of astrocyte swelling/brain edema following TBI is not known.…”

mentioning

confidence: 99%

Activation of NF-κB Mediates Astrocyte Swelling and Brain Edema in Traumatic Brain Injury

Jayakumar

Tong

Ruíz-Cordero

et al. 2014

Journal of Neurotrauma

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Brain edema and associated increased intracranial pressure are major consequences of traumatic brain injury (TBI). While astrocyte swelling (cytotoxic edema) represents a major component of the brain edema in the early phase of TBI, its mechanisms are unclear. One factor known to be activated by trauma is nuclear factor-jB (NF-jB). Because this factor has been implicated in the mechanism of cell swelling/brain edema in other neurological conditions, we examined whether NF-jB might also be involved in the mediation of post-traumatic astrocyte swelling/brain edema. Here we show an increase in NF-jB activation in cultured astrocytes at 1 and 3 h after trauma (fluid percussion injury, FPI), and that BAY 11-7082, an inhibitor of NF-jB, significantly blocked the trauma-induced astrocyte swelling. Increased activities of nicotinamide adenine dinucleotide phosphate-oxidase and the Na + , K + , 2Cl -cotransporter were also observed in cultured astrocytes after trauma, and BAY 11-7082 reduced these effects. We also examined the role of NF-jB in the mechanism of cell swelling by using astrocyte cultures derived from transgenic (Tg) mice with a functional inactivation of astrocytic NF-jB. Exposure of cultured astrocytes from wild-type mice to in vitro trauma (3 h) caused a significant increase in cell swelling. By contrast, traumatized astrocyte cultures derived from NF-jB Tg mice showed no swelling. We also found increased astrocytic NF-jB activation and brain water content in rats after FPI, while BAY 11-7082 significantly reduced such effects. Our findings strongly suggest that activation of astrocytic NF-jB represents a key element in the process by which cytotoxic brain edema occurs after TBI.

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“…In a study done by Human T in 2012, Conivaptan was useful in patients with acute Hyponatremia after traumatic brain injury [10]. In a study of Katada R on mice Ethanol, after head injury caused an increase in cerebral edema & Hyponatremia [11].…”

Section: Resultsmentioning

confidence: 99%