Current status of cerebral protection with mild-to-moderate hypothermia after traumatic brain injury

Jiang, Jiyao; Yang, Xiaofeng

doi:10.1097/mcc.0b013e32807f2a80

Cited by 29 publications

(24 citation statements)

References 13 publications

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“…The thus termed "therapeutic hypothermia" provides neuroprotection for patients after a cardiac arrest, stroke, or spinal cord or head injuries (Cheung et al, 2006;Jiang and Yang, 2007;den Hertog et al, 2009) through several mechanisms that include reduction in brain metabolic rate, effects on cerebral blood flow, reduction of the critical threshold for oxygen delivery, blockade of excitotoxic mechanisms, calcium antagonism, preservation of protein synthesis, reduction of brain thermopooling, a decrease in edema formation, modulation of the inflammatory response, neuroprotection of the white and gray matter, and modulation of apoptotic cell death (Froehler and Geocadin, 2007). The acute management of these patients is a major challenge and determines the long-term clinical outcome.…”

Section: Discussionmentioning

confidence: 99%

Paracetamol-Induced Hypothermia Is Independent of Cannabinoids and Transient Receptor Potential Vanilloid-1 and Is Not Mediated by AM404

Ayoub

Pryce²,

Seed³

et al. 2011

Drug Metabolism and Disposition

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ABSTRACT:In recent years, there has been increasing interest in hypothermia induced by paracetamol for therapeutic purposes, which, in some instances, has been reported as a side effect. Understanding the mechanism by which paracetamol induces hypothermia is therefore an important question. In this study, we investigated whether the novel metabolite of paracetamol, N-(4-hydroxyphenyl)arachidonylamide (AM404), which activates the cannabinoid (CB) and transient receptor potential vanilloid-1 (TRPV1) systems, mediates the paracetamolinduced hypothermia. The hypothermic response to 300 mg/kg paracetamol in CB 1 receptor (CB 1 R) and TRPV1 knockout mice was compared to wild-type mice. Hypothermia induced by paracetamol was also investigated in animals pretreated with the CB 1 R or TRPV1 antagonist 1-(2,4-dichlorophenyl)-5-(4-iodophenyl)-4-methyl-N-1-piperdinyl-1H-pyrazole-3-carboxamide trifluoroacetate salt (AM251) or 4-chloro-3-methoxycinnamanilide (SB366791), respectively. In CB 1 R or TRPV1 knockout mice, paracetamol induced hypothermia to the same extent as in wild-type mice. In addition, in C57BL/6 mice pretreated with AM251 or SB366791, paracetamol induced hypothermia to the same extent as in control mice. AM404 failed to induce hypothermia at pharmacological doses. Inhibition of fatty acid amide hydrolase (FAAH), which is involved in the metabolism of paracetamol to AM404, did not prevent the development of hypothermia with paracetamol. Paracetamol also induced hypothermia in FAAH knockout mice to the same extent as wild-type mice. We conclude that paracetamol induces hypothermia independent of cannabinoids and TRPV1 and that AM404 does not mediate this response. In addition, potential therapeutic value of combinational drug-induced hypothermia is supported by experimental evidence.

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Section: Discussionmentioning

confidence: 99%

Paracetamol-Induced Hypothermia Is Independent of Cannabinoids and Transient Receptor Potential Vanilloid-1 and Is Not Mediated by AM404

Ayoub

Pryce²,

Seed³

et al. 2011

Drug Metabolism and Disposition

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“…In a recent observational study of ICP after TBI, only one-third of patients achieved their highest ICP within the first 2 days after injury, and 20% did not achieve their peak ICP until after day 5. 20 A number of studies have reported a rebound increase in ICP associated with the discontinuation of cooling, 17,25,26,[35][36][37] perhaps negating any benefit accrued during the first 48 hours of cooling. In earlier studies, a 24-48 hour duration of cooling was chosen because of concerns that longer periods of hypothermia would be associated with increased risk of adverse events.…”

Section: Discussionmentioning

confidence: 99%

Prophylactic hypothermia for traumatic brain injury: a quantitative systematic review

Fox

Doyle‐Waters

et al. 2010

CJEM

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Introduction: During the past 7 years, considerable new evidence has accumulated supporting the use of prophylactic hypothermia for traumatic brain injury (TBI). Studies can be divided into 2 broad categories: studies with protocols for cooling for a short, predetermined period (e.g., 24-48 h), and those that cool for longer periods and/or terminate based on the normalization of intracranial pressure (ICP). There have been no systematic reviews of hypothermia for TBI that include this recent new evidence. Methods: This analysis followed the recommendations of the Cochrane Handbook for Systematic Reviews of Interventions and the QUOROM (quality of reporting of meta-analyses) statement. We developed a comprehensive search strategy to identify all randomized controlled trials (RCTs) comparing therapeutic hypothermia with standard management in TBI patients. We searched Embase, MEDLINE, Web of Science, the Cochrane Central Register of Controlled Trials, the Cochrane Database of Systematic Reviews, ProceedingsFirst and PapersFirst. Additional relevant articles were identified by hand-searching conference proceedings and bibliographies. All stages of study identification and selection, quality assessment and analysis were conducted according to prospectively defined criteria. Study quality was determined by assessment of each study for the use of allocation concealment and outcome assessment blinding. Studies were divided into 2 a priori-defined subgroups for analysis based on cooling strategy: short term (≤ 48 h), and long term or goal-directed (> 48 h and/or continued until normalization of ICP). Outcomes included mortality and good neurologic outcome (defined as Glasgow Outcome Scale score of 4 or 5). Pooling of primary outcomes was completed using relative risk (RR) and reported with 95% confidence intervals (CIs). Results: Of 1709 articles, 12 studies with 1327 participants were selected for quantitative analysis. Eight of these studies cooled according to a long-term or goal-directed strategy, and 4 used a short-term strategy. Summary results demonstrated lower mortality (RR 0.73, 95% CI 0.62-0.85) and more

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“…The duration of hypothermia therapy can vary widely depending upon the clinical needs of the individual patient; reports in the literature range from 24 hours to 14 days (McIntyre et al 2003). The rewarming phase of therapy is critical due to the risk of mitochondrial injury, vascular dysregulation, and rebound increases in ICP (Jiang, Yu, & Zhu 2000;Jiang & Yang 2007;Povlishock & Wei 2009). Although the optimum rewarming rate has yet to be determined, most authors advocate rates of approximately 0.5-1 o /hour (Bernard & Buist 2003;Bernard et al 2002;Alzaga, Cerdan, & Varon 2006).…”

Section: Cerebral Edema Intracranial Hypertension and Cerebral Perfumentioning

confidence: 99%

Traumatic Brain Injury - Acute Care

Hays¹,

Varma²

2012

Brain Injury - Pathogenesis, Monitoring, Recovery and Management

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Current status of cerebral protection with mild-to-moderate hypothermia after traumatic brain injury

Abstract: Mild-to-moderate hypothermia plays a significant role in cerebral protection after traumatic brain injury.

Cited by 29 publications

References 13 publications

Paracetamol-Induced Hypothermia Is Independent of Cannabinoids and Transient Receptor Potential Vanilloid-1 and Is Not Mediated by AM404

Paracetamol-Induced Hypothermia Is Independent of Cannabinoids and Transient Receptor Potential Vanilloid-1 and Is Not Mediated by AM404

Prophylactic hypothermia for traumatic brain injury: a quantitative systematic review

Traumatic Brain Injury - Acute Care

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