Hypothermia Therapy for Brain Injury

Diller, Kenneth R.; Zhu, Liang

doi:10.1146/annurev-bioeng-061008-124908

Cited by 51 publications

(55 citation statements)

References 167 publications

(185 reference statements)

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“…The current study supports this finding, indicating reduced damage to these structures in rats treated with hypothermic treatments compared to those allowed to recover at normal body temperatures. Recently, Diller and Zhu (2009) reviewed a large body of articles linking formation of harmful factors to poor prognosis in TBI, highlighting the value of MIH in mediating many of these compounds. Consistent with these reports, the current study indicated that BACE expression after TBI was significantly reduced by hypothermia intervention.…”

Section: Figmentioning

confidence: 99%

Effects of Mild Hypothermia Treatment on Rat Hippocampal β-Amyloid Expression Following Traumatic Brain Injury

Cheng

Zhang²,

Sun³

et al. 2013

Therapeutic Hypothermia and Temperature Management

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Previous studies have reported that mild induced hypothermia (MIH) treatment has positive effects on traumatic brain injury (TBI) outcomes, which have recently been linked to b-amyloid (Ab)-induced secondary brain injury (SBI) extent in hippocampal tissues. We therefore investigate the relationship between MIH treatment and expression of Ab and related proteins following TBI. Adult Sprague-Dawley rats were randomly divided into three equal groups (S: sham-operated, N: normothermia, and H: mild hypothermia). After TBI induced by fluid percussion, group N remained at normal temperature, and group H underwent MIH (32°C) for 6 hours. Behavioral scale scores were then assessed. All rats were sacrificed 24 hours and hippocampal tissues were harvested, stained with hematoxylin and eosin. mRNA and protein expressions of Ab, b-amyloid protein precursor (APP), and b-secretase (BACE) were analyzed. Our results revealed significantly improved behavioral scale scores and the surviving neuron numbers were observed in group H compared to group N ( p < 0.05). Additionally, group N increased APP, Ab, and BACE levels compared to group S (all p < 0.05). Reduced expression of APP-, Ab-, and BACE were apparent in group H compared to group N (all p < 0.05). However, no statistically significant difference was observed between groups H and S in behavioral scale scores and the expression of APP-, Ab-, and BACE ( p > 0.05). In conclusion, MIH treatment significantly improves the survival of neuron and reduced Ab, BACE, and APP upregulation after TBI, which may provide a better understanding of the mechanisms by which hypothermia reduces SBI in TBI patients.

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Section: Figmentioning

confidence: 99%

Effects of Mild Hypothermia Treatment on Rat Hippocampal β-Amyloid Expression Following Traumatic Brain Injury

Cheng

Zhang²,

Sun³

et al. 2013

Therapeutic Hypothermia and Temperature Management

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show abstract

“…14 Briefly, male Wistar rats or C57/Bl6 male mice (Harlan, Udine, Italy) were killed under isoflurane-induced anesthesia and their hippocampi were rapidly removed and placed in ice-cold oxygenated (95% O 2 to 5% CO 2 ) artificial cerebrospinal fluid (ACSF). Rats brains and slices were maintained in ACSF containing (in mmol/L): NaCl 125, KCl 3, NaH 2 PO 4 1.25, MgSO 4 10. Parasagittal rat or mouse hippocampal slices (400 mm thick) were prepared using a McIlwain tissue chopper (The Mickle Lab.…”

Section: Hippocampal Field Excitatory Postsynaptic Potential Recordingmentioning

confidence: 99%

“…[1][2][3] Yet, current cooling devices suffer from excessive degree of invasiveness and/or considerable delay in inducing the hypothermic effects. 4,5 Because of that, drugs triggering rapid and safe hypothermia could be of remarkable relevance to treatment of different neurological disorders. These tools could also be of therapeutic significance in conditions of altered thermoregulation such as febrile illness, drug-induced hyperthermia, or heat stroke.…”

Section: Introductionmentioning

confidence: 99%

Neurological Basis of AMP-Dependent Thermoregulation and its Relevance to Central and Peripheral Hyperthermia

Muzzi

Blasi

Masi

et al. 2012

J Cereb Blood Flow Metab

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Therapeutic hypothermia is of relevance to treatment of increased body temperature and brain injury, but drugs inducing selective, rapid, and safe cooling in humans are not available. Here, we show that injections of adenosine 5 0 -monophosphate (AMP), an endogenous nucleotide, promptly triggers hypothermia in mice by directly activating adenosine A1 receptors (A1R) within the preoptic area (POA) of the hypothalamus. Inhibition of constitutive degradation of brain extracellular AMP by targeting ecto 5 0 -nucleotidase, also suffices to prompt hypothermia in rodents. Accordingly, sensitivity of mice and rats to the hypothermic effect of AMP is inversely related to their hypothalamic 5 0 -nucleotidase activity. Single-cell electrophysiological recording indicates that AMP reduces spontaneous firing activity of temperature-insensitive neurons of the mouse POA, thereby retuning the hypothalamic thermoregulatory set point towards lower temperatures. Adenosine 5 0 -monophosphate also suppresses prostaglandin E2-induced fever in mice, having no effects on peripheral hyperthermia triggered by dioxymetamphetamine (ecstasy) overdose. Together, data disclose the role of AMP, 5 0 -nucleotidase, and A1R in hypothalamic thermoregulation, as well and their therapeutic relevance to treatment of febrile illness.

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“…4,5 Indeed, tools that selectively prompt transient cooling of body temperature (Tb) and avoid negative side effects or suspended animation are not available in humans. 6 In this respect, injection of the endogenous nucleotide 5 0 -adenosine monophosphate (AMP) induces profound and transient hypothermia in rodents.…”

Section: Introductionmentioning

confidence: 99%

AMP-Dependent Hypothermia Affords Protection from Ischemic Brain Injury

Muzzi¹,

Blasi²,

Chiarugi

2012

J Cereb Blood Flow Metab

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In light of the relevance of therapeutic hypothermia to stroke treatment, we investigated whether 5 0 -adenosine monophosphate (AMP)-dependent cooling affords protection from ischemic brain injury. We show that hypothermia by AMP is because of adenosine A1 receptor (A1R) activation and is not invariantly associated with hypotension. Inhibition of ecto-5 0 -nucleotidasedependent constitutive degradation of brain extracellular AMP by methylene-ADP (AMPCP) also suffices to prompt A1R-dependent hypothermia without hypotension. Both intraischemic and postischemic hypothermia by AMP or AMPCP reduce infarct volumes and mortality of mice subjected to transient middle cerebral artery occlusion. Data disclose that AMP-dependent hypothermia is of therapeutic relevance to treatment of brain ischemia.

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Hypothermia Therapy for Brain Injury

Cited by 51 publications

References 167 publications

Effects of Mild Hypothermia Treatment on Rat Hippocampal β-Amyloid Expression Following Traumatic Brain Injury

Effects of Mild Hypothermia Treatment on Rat Hippocampal β-Amyloid Expression Following Traumatic Brain Injury

Neurological Basis of AMP-Dependent Thermoregulation and its Relevance to Central and Peripheral Hyperthermia

AMP-Dependent Hypothermia Affords Protection from Ischemic Brain Injury

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