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Treatment of Acute Ischemic Stroke with Calcium Antagonists

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Part of the book series: Medical Science Symposia Series ((MSSS,volume 3))

Abstract

Calcium exerts normal physiologic functions as a membrane stabilizer, metabolic regulator, and second messenger. However, it also can be involved in anoxic and toxic cell death (1). In animal models of global brain ischemia, which try to mimic the cerebral sequelae of cardiac arrest, loss of cellular calcium homeostasis has been related to: (a) selective neuronal necrosis, presumably in neurons with a higher density of calcium channels; and (b) delayed neuronal death, ascribed to cytosolic calcium overload. Similar pathologic processes have been assumed for neuronal tissue at risk in the “ischemic penumbra,” i.e., an area of reversibly damaged brain tissue surrounding an irreversibly necrotic core in thrombotic stroke. The hypothesis of calcium-induced cell damage implies that pathological increases in cytosolic calcium concentration produce cell damage and death by causing enhanced lipolysis and proteolysis, energy wastage, activation of protein kinases, and altered gene expression. From this, a strategy for acute treatment of ischemic cerebrovascular accidents with calcium antagonists has been developed. However, at the present time this treatment strategy has not yet been fully confirmed by the results from clinical trials with calcium antagonists in stroke. It is not clear whether this discrepancy is due to incomplete or incorrect insight in pathogenetic mechanisms of ischemic stroke, or to methodological problems in the clinical trials.

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© 1993 Springer Science+Business Media Dordrecht

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Gheuens, J., De Ryck, M., Van Reempts, J., Peters, T. (1993). Treatment of Acute Ischemic Stroke with Calcium Antagonists. In: Godfraind, T., Paoletti, R., Govoni, S., Vanhoutte, P.M. (eds) Calcium Antagonists. Medical Science Symposia Series, vol 3. Springer, Dordrecht. https://doi.org/10.1007/978-94-011-1725-8_35

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  • DOI: https://doi.org/10.1007/978-94-011-1725-8_35

  • Publisher Name: Springer, Dordrecht

  • Print ISBN: 978-94-010-4756-2

  • Online ISBN: 978-94-011-1725-8

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