In addition to slowing oxygen consumption , posttraumatic and ischemic hypothermia has been reported to blunt the rise in extracellular levels of excitatory amino acids after parasagittal F-P injury [1, 2, 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 . In a model of spinal cord ischemia, hypothermia effectively attenuated extracellular glutamate release . Wakamatsu and colleagues  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 .
KeywordsMiddle Cerebral Artery Occlusion Excitatory Amino Acid Therapeutic Hypothermia Glutamate Concentration Spinal Cord Ischemia
- 1.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 65:1704–1711Google Scholar
- 7.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–H1775Google Scholar
- 8.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 88:56–62PubMedGoogle Scholar