The Effect of Brain Temperature on Acute Inflammation after Traumatic Brain Injury in Rats

Whalen, Michael J.; Carlos, Timothy M.; Clark, Robert S. B.; Marion, Donald W.; DeKosky, Steven T.; Heineman, Scott; Schiding, Joanne K.; Memarzadeh, Farnaz; Kochanek, Patrick M.

doi:10.1089/neu.1997.14.561

Cited by 80 publications

(33 citation statements)

References 58 publications

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“…Hyperthermia is also known to increase extracellular glutamate levels, neurotoxic zinc translocation, and potentiate inflammatory signaling to increase neuronal death (Sharma, 2006; Suehiro et al, 1999; Suh et al, 2006; Takagi et al, 1994). In particular, infiltration of inflammatory cells is aggravated by hyperthermia (Chatzipanteli et al, 2000; Thompson et al, 2005; Whalen et al, 1997). The increase in inflammation may have contributed to neuronal death in structures involved in the formation of long-term memories for these particular learning tasks (Sakurai et al, 2012; Suzuki et al, 2004).…”

Section: Discussionmentioning

confidence: 99%

Emergence of cognitive deficits after mild traumatic brain injury due to hyperthermia

Titus

Furones

Atkins

et al. 2015

Experimental Neurology

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Mild elevations in core temperature can occur in individuals involved in strenuous activities that are risky for potentially sustaining a mild traumatic brain injury (mTBI) or concussion. Recently, we have discovered that mild elevations in brain temperature can significantly aggravate the histopathological consequences of mTBI. However, whether this exacerbation of brain pathology translates into behavioral deficits is unknown. Therefore, we investigated the behavioral consequences of elevating brain temperature to mildly hyperthermic levels prior to mTBI. Adult male Sprague Dawley rats underwent mild fluid-percussion brain injury or sham surgery while normothermic (37 °C) or hyperthermic (39 °C) and were allowed to recover for 7 days. Animals were then assessed for cognition using the water maze and cue and contextual fear conditioning. We found that mTBI alone at normothermia had no effect on long-term cognitive measures whereas mTBI animals that were hyperthermic for 15 min prior to and for 4 h after brain injury were significantly impaired on long-term retention for both the water maze and fear conditioning. In contrast, hyperthermic mTBI animals cooled within 15 min to normothermia demonstrated no significant long-term cognitive deficits. Mild TBI irrespective of temperature manipulations resulted in significant short-term working memory deficits. Cortical atrophy and contusions were detected in all mTBI treatment groups and contusion volume was significantly less in hyperthermic mTBI animals that were cooled as compared to hyperthermic mTBI animals that remained hyperthermic. These results indicate that brain temperature is an important variable for mTBI outcome and that mildly elevated temperatures at the time of injury result in persistent cognitive deficits. Importantly, cooling to normothermia after mTBI prevents the development of long-term cognitive deficits caused by hyperthermia. Reducing temperature to normothermic levels soon after mTBI represents a rational approach to potentially mitigate the long-term consequences of mTBI.

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Section: Discussionmentioning

confidence: 99%

Emergence of cognitive deficits after mild traumatic brain injury due to hyperthermia

Titus

Furones

Atkins

et al. 2015

Experimental Neurology

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“…Hypothermia exerts its beneficial effects not merely by reducing oxygen requirement (uptake) (18,46) but through the synergism of multiple mechanisms, such as preservation of adenosine 5'-triphosphate (47) and reduction of excitotoxicity (48), edema (49), free radical reactions (50), and inflammation (51,52). Protective-preservative profound or ultraprofound hypothermia during CA 60 -180 mins, induced with CPB before the insult, in animals, has been reported previously by us (20 -22) and others (23)(24)(25)(26)(27)(28)(29)(30).…”

Section: Discussionmentioning

confidence: 99%

Survival without brain damage after clinical death of 60–120 mins in dogs using suspended animation by profound hypothermia*

Behringer

Šafář

et al. 2003

Critical Care Medicine

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112

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In a systematic series of studies in dogs, the rapid induction of profound cerebral hypothermia (tympanic temperature 10 degrees C) by aortic flush of cold saline immediately after the start of exsanguination cardiac arrest-which rarely can be resuscitated effectively with current methods-can achieve survival without functional or histologic brain damage, after cardiac arrest no-flow of 60 or 90 mins and possibly 120 mins. The use of additional preservation strategies should be pursued in the 120-min arrest model.

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“…The mechanisms underlying the beneficial effects of posttraumatic hypothermia are multifactorial and include excitotoxicity, calciumdependent intercellular signaling, apoptosis, and edema formation (Dietrich and Bramlett, 2010;Yenari and Han, 2012). In addition, hypothermia has been reported to attenuate various inflammatory events including proinflammatory gene expression and protein levels when compared with normothermic TBI in some (Chatzipanteli et al, 2000;Goss et al, 1995;Kinoshita et al, 2002;Lotocki et al, 2006;Marion et al, 1997;Vitarbo et al, 2004;Whalen et al, 1997) but not all studies (Buttram et al, 2007;Truettner et al, 2005). Thus, a current area of research is directed to the continued investigation of the cellular and molecular events associated with the beneficial effects of hypothermia on posttraumatic inflammatory processes.…”

Section: Introductionmentioning

confidence: 99%

Effects of Therapeutic Hypothermia on Inflammasome Signaling after Traumatic Brain Injury

Tomura

Vaccari

Keane

et al. 2012

J Cereb Blood Flow Metab

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Traumatic brain injury (TBI) activates the NALP1/NLRP1 inflammasome, which is an important component of the early innate inflammatory response to injury. We investigated the influence of therapeutic hypothermia on inflammasome activation after TBI. Adult male Sprague-Dawley rats were subjected to moderate fluid percussion brain injury. Temperature manipulation (331C or 371C) was initiated 30 minutes after TBI and maintained for 4 hours. At 4 or 24 hours after TBI, traumatized cortex and hippocampus were prepared for immunoblot or immunohistochemical analysis. In the normothermic groups, caspase-1, caspase-11 and expression of the purinergic receptor P2X7 increased at 24 hours after TBI. Posttraumatic hypothermia lead to decreased expression of these proteins at 24 hours compared with normothermic levels. Immunocytochemical studies showed that posttraumatic hypothermia also decreased caspase-1 staining in cerebral cortical neurons compared with normothermic TBI. Cultured cortical neurons subjected to stretch injury demonstrated significant secretion of caspase-1 into the culture medium and caspase-3 activation, both results reduced by hypothermic treatment. Posttraumatic hypothermia decreases inflammasome signaling in neurons and reduces the innate immune response to TBI at 24 hours after injury. Therapeutic hypothermia may protect the injured central nervous system by targeting the detrimental consequences of the innate immune response to injury.

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The Effect of Brain Temperature on Acute Inflammation after Traumatic Brain Injury in Rats

Cited by 80 publications

References 58 publications

Emergence of cognitive deficits after mild traumatic brain injury due to hyperthermia

Emergence of cognitive deficits after mild traumatic brain injury due to hyperthermia

Survival without brain damage after clinical death of 60–120 mins in dogs using suspended animation by profound hypothermia*

Effects of Therapeutic Hypothermia on Inflammasome Signaling after Traumatic Brain Injury

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