Abstract
Calcium entry blockers stabilize voltage-dependent calcium channels within cell membranes and prevent abnormal intracellular entry of calcium (Ca2+) through endothelial and ischemic neuronal cell membranes [9, 30]. It is well known that when Ca2+ ions enter vascular smooth muscle, contraction results, but if calcium entry is blocked by calcium antagonists, vascular dilatation occurs. It is also well known that when extracellular Ca2+ moves into ischemic neurones, neuronal function initially becomes impaired, eventually followed by neuronal death as excessive intracellular Ca2+ interferes with intracellular messengers and mitochondrial metabolism [31]. Experimental studies of cerebral ischemia in animal models have shown that pretreatment with the calcium entry antagonist nimodipine results in protection of the brain from cerbral infarction by preventing calcium entry into ischemic neurones and glia [1].
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© 1994 Springer-Verlag Berlin Heidelberg
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Meyer, J.S., Takashima, S., Terayama, Y. (1994). Calcium Channel Blockers Prevent Delayed Cerebral Ischemia After Intracranial Aneurysmal Subarachnoid Hemorrhage. 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_12
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