Abstract
Considerable data support the point of view that calcium antagonists, whether given before the onset of ischemia or exactly at the time of reperfusion, ameliorate stunning. Benefit after the onset of reperfusion is much more controversial. It is proposed that the mechanisms whereby calcium antagonists act vary between these situations. When given before or at the onset of ischemia, then an antiischemic effect is likely. According to the hypothesis that the severity of ischemic damage determines the severity of reperfusion damage, the calcium antagonists indirectly lessen reperfusion damage. When given exactly at the time of reperfusion, the proposal is that the calcium antagonists are specifically limiting the entry of calcium ions via the calcium channel and thereby diminishing pathogenic cytosolic calcium oscillations. The reported benefit of calcium antagonists when given postreperfusion to the heart in situ, in the presence of established stunning, is of unknown mechanism and controversial significance. The hypothesis of a two-stage model of stunning with calcium as a pathogen is in accord with most of the available evidence.
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