Calcium Antagonists and Ischaemia: A Critical Evaluation

  • W. G. Nayler
Conference paper


The development of reliable reperfusion techniques, coupled with the introduction of effective, nontoxic thrombolytic agents has revived interest in the feasibility of restoring function to cardiac muscle which otherwise would die and necrose [1]. As a result, attention is again being focused on the precise determinants and time of onset of irreversible injury [2], the possible involvement of free radicals [3], the significance of cell swelling [4], of adenosine triphosphate and adenosine precursor depletion [2] and the relevance of the “Ca2+ overload” phenomenon. As far as the Ca2+ overload phenomenon is concerned, whilst it is firmly established that hearts which are reperfused after more than a few minutes of ischemia gain Ca2+ in an apparently uncontrolled manner [5] the precise cause of this gain, its time course, the route of Ca2+ entry, and the significance of the gain remain the subject of debate and controversy [6]. As far as the significance of the gain is concerned there are two distinct possibilities which warrant consideration. Some investigators argue that the Ca2+ gain which occurs upon reperfusion begins only after the onset of irreversible injury, so that although the additional Ca2+ may hasten the expression of the injury it is not a precipitating or primary factor. The alternative hypothesis is that the Ca2+ gain which occurs upon reperfusion actually triggers the cascade of events which culminates in irreversible injury.


Infarct Size Calcium Antagonist Ischaemic Event Calcium Entry Blocker Occlusive Event 
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© Springer-Verlag Berlin Heidelberg 1989

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  • W. G. Nayler

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