Abstract
Extensive experimental evidence has confirmed that the early events of ischemia-induced neuronal damage are characterized by excessive influx of calcium [13, 14]. Activation of calcium-dependent enzymes such as protein kinase C, calmodulin (CaM) kinase II, calpain I, calcineurin, and phospholipase A2 is believed to play a major role in neuronal excitotoxicity [2, 4, 5, 16]. In addition, therapeutic intervention with agents which target either voltage- or receptor-mediated ion channels are found to have neuroprotective affects in animal models of focal and global ischemia [6, 7, 12, 14]. Despite these findings, the results of clinical therapeutic trials using these agents have thus far been inconclusive in human stroke patients [1]. Possible explanations for these results include differences in vulnerability between human and animal neurons, lower dose tolerance due to coexisting cardiovascular disease, and insensitivity in methods of detecting modest neuronal protection in humans.
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© 1994 Springer-Verlag Berlin Heidelberg
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De Graba, T.J., Grotta, J.C. (1994). Threshold of Calcium Influx After Global and Focal Ischemia: Implications for the Window of Therapeutic Opportunity. In: Hartmann, A., Yatsu, F., Kuschinsky, W. (eds) Cerebral Ischemia and Basic Mechanisms. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-78151-3_15
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DOI: https://doi.org/10.1007/978-3-642-78151-3_15
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