Abstract
In addition to slowing oxygen consumption [5], posttraumatic and ischemic hypothermia has been reported to blunt the rise in extracellular levels of excitatory amino acids after parasagittal F-P injury [1–3]. However, in a model of controlled cortical impact, hypothermia failed to attenuate the rise in extracellular aspartate and glutamate although contusion volume was significantly reduced by cooling [4]. In a model of spinal cord ischemia, hypothermia effectively attenuated extracellular glutamate release [6]. Wakamatsu and colleagues [8] reported that intraischemic moderate hypothermia (32°C) significantly reduced glutamate concentrations of intrathecal dialysate and improved neurologic status and histopathology after spinal cord ischemia. In contrast, other reports have indicated that hypothermia did not attenuate extracellular accumulation of excitatory amino acids or improve energy metabolism. For example, hyperthermia (39°C) during middle cerebral artery occlusion led to increased levels of extracellular glutamate compared to normothermic animals [7].
Access this chapter
Tax calculation will be finalised at checkout
Purchases are for personal use only
References
Globus MY-T, Alonso O, Dietrich WD, Busto R, Ginsberg MD (1995) Glutamate release and free radical production following brain injury: effects of posttraumatic hypothermia. J Neurotrauma 65:1704–1711
Globus MY-T, Busto R, Lin B, Schnippering H, Ginsberg MD (1995) Detection of free radical activity during transient global ischemia and recirculation: effects of intraischemic brain temperature modulation. J Neurochem 65:1250–1256
Goss JR, Styren SD, Miller PD, Kochanek PM, Palmer AM, Graenen G, Jeftinija S, Grants I, Lucas JH (1996) The role of excitatory amino acids in hypothermic injury to mammalian spinal cord neurons. J Neurotrauma 13:809–818
Palmer AM, Marion DW, Botsceller ML, Redd EE (1993) Therapeutic hypothermia is cytoprotective without attenuating the traumatic brain injury-induced elevations in interstitial concentrations of aspartate and glutamate. J Neurotrauma 10:363–372
Rosomoff HL, Holaday S (1954) Cerebral blood flow and cerebral oxygen consumption during hypothermia. Am J Physiol 179:85–88
Saganova K, Marsala M (1994) Intrathecal administration of dizocilpine maleate (MK-801) attenuates ischemic damage in the rabbit spinal cord. Exp Neurol 130:337–343
Tagaki K, Ginsberg MD, Globus MY-T, Martinez E, Busto R (1994) Effect of hyperthermia on glutamate release in ischemic penumbra after middle cerebral artery occlusion in rats. Am Physiol Soc H1770–H1775
Wakamatsu H, Matsumoto M, Nakakimura K, Sakabe T (1999) The effects of moderate hypothermia and intrathecal tetracaine on glutamate concentrations of intrathecal dialysate and neurologic and histopathologic outcome in transient spinal cord ischemia in rabbits. Anesth Analg 88:56–62
Author information
Authors and Affiliations
Rights and permissions
Copyright information
© 2004 Springer Japan
About this chapter
Cite this chapter
Hayashi, N., Dietrich, D.W. (2004). Excitotoxicity. In: Brain Hypothermia Treatment. Springer, Tokyo. https://doi.org/10.1007/978-4-431-53953-7_13
Download citation
DOI: https://doi.org/10.1007/978-4-431-53953-7_13
Publisher Name: Springer, Tokyo
Print ISBN: 978-4-431-67964-6
Online ISBN: 978-4-431-53953-7
eBook Packages: Springer Book Archive