Abstract
Numerous experimental data suggest that the excitatory amino acid neurotransmitter glutamate is involved in the pathophysiology of ischaemic neuronal injury [8] as well as traumatic brain injury [3], and that the glutamate subtype receptor, N-methyl-D-aspartate (NMDA) antagonists have cytoprotective effect against ischaemic neuronal damage [6]. Since secondary ischaemia is one of the major contributing factors in the pathology of traumatic injury of the brain and patients with head injury can arrive at a hospital at a time before the development of secondary ischaemia, it can be a promising therapeutic area for NMDA antagonists. However, many patients with severe head injury suffer from respiratory problems such as apnea, atelectasis and aspiration in acute stage, while in animal experiment an optimal physiological state has been emphasized. The objective of this study was to examine the effect of systemic acidosis induced by respiratory depression under halothane anesthesia upon the extent of ischaemic brain damage as well as upon the cytoprotective efficacy of the competitive NMDA receptor antagonist, (E)-4-(3-phosphonoprop-2-enyl)-piperazine-2-carboxylic acid(D-CPPene) in the middle cerebral artery occlusion (MCAO) model of rats.
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© 1993 Springer-Verlag Berlin Heidelberg
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Park, C.K., McCulloch, J., Kang, J.K., Choi, C.R. (1993). Effects of Respiratory Depression on Cytoprotective Effect of the Competitive NMDA Antagonist, D-CPPene. In: Avezaat, C.J.J., van Eijndhoven, J.H.M., Maas, A.I.R., Tans, J.T.J. (eds) Intracranial Pressure VIII. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-77789-9_36
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DOI: https://doi.org/10.1007/978-3-642-77789-9_36
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