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Hypothesis-generating for gap junction-targeted reperfusion therapy; leaves open clinical translation to infarct size reduction.
During myocardial reperfusion, increased cytosolic Ca(2+) concentration may cause hypercontracture and cell death. Hypercontracture can propagate to adjacent cells by a gap junction-dependent mechanism. This propagation explains infarct geometry and increases the final extent of necrosis. Its prevention may represent a new therapeutic strategy for treating patients with myocardial infarction.
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García‐Dorado et al. (2000) studied this question.
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