Abstract
Calcium channel blockers have the potential to attenuate ischaemic brain damage via a number of distinct mechanisms. Voltage-dependent Ca2+ channels are present on cerebrovascular smooth muscle and their blockade results in relaxation. Calcium channel blockers are thus capable of improving cerebral tissue perfusion in ischaemic tissue, to levels above those associated with neuronal damage. Alternatively, or additionally, calcium channel blockers, by limiting the influx of calcium into neurones, might prevent the chain of intracellular events which calcium initiates (protease and lipase activation, mitochondrial dysfunction, etc.) and which leads ultimately to irreversible ischaemic cell damage (for reviews see Siesjö 1981; Greenberg 1987). In this review, we consider the evidence that calcium channel blockers are capable of influencing the amount of ischaemic brain damage in animal models of focal cerebral ischaemia and the extent to which improved perfusion or blockade of neuronal Ca2+ entry contributes to any amelioration. The review is based on published reports of the effects of nimodipine in the rat from our laboratory (Mohamed et al. 1984, 1985 a, b; Gotoh et al. 1986).
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© 1989 Springer-Verlag Berlin Heidelberg
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McCulloch, J., Graham, D.I., Harper, A.M., Teasdale, G.M. (1989). Calcium Antagonists and Experimental Focal Cerebral Ischemia. In: Hartmann, A., Kuschinsky, W. (eds) Cerebral Ischemia and Calcium. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-85863-5_23
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DOI: https://doi.org/10.1007/978-3-642-85863-5_23
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