Patterns of Excitatory Amino Acid Release and Ionic Flux After Severe Human Head Trauma
In many of the conditions that result in acute cerebral damage, the role of excitatory amino acids has become the focus of current investigation [1, 2]. The demonstration of excitatory amino acid release has been shown in several animal models of brain trauma, and has been associated with both structural damage and metabolic abnormalities [3–5]. These changes may be reversed by administration of excitatory amino acid antagonists, and this group of compounds has shown a greater magnitude of neuroprotective effect than any other series of drugs in the laboratory [3, 6]. As part of an ongoing study, we have recently measured release of excitatory amino acids (EAAs) and ions in 17 acutely head-injured patients in our institution, with the aim of determining the circumstances that are responsible for glutamate release and their possible role as an exacerbating factor in causing secondary brain damage after severe human head injury.
KeywordsCerebral Perfusion Pressure Mean Arterial Blood Pressure Excitatory Amino Acid Secondary Insult Acute Subdural Hematoma
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- 3.Bullock R, Fujisawa H (1992) The role of glutamate antagonists for the treatment of CNS injury. J Neurotrauma 9: 5443–5461Google Scholar
- 7.Tsuji O, Marmarou A, Bullock R (1994) Microdialysis detection of eletrolytes and amino acid changes following head impact acceleration, coupled with secondary insult. In: 9th International Symposium on Intracranial Pressure (in press)Google Scholar
- 9.Bullock R, Stout A, Woodward JJ, Tsuji O, Marmarou A, Young HF (1994) EAA release in severe human head trauma: the role of intracranial pressure and cerebral perfusion changes. In: 9th International Symposium on Intracranial Pressure (in press)Google Scholar