Abstract
To the Editor: A recent article in Circulation 1 proposes that prevention of myocardial damage by postconditioning involves the inhibition of mitochondrial permeability transition pore (mPTP) opening. We find the idea attractive and in keeping with studies implicating mPTP in postischemic damage2 but believe this study is too preliminary to prove this hypothesis. The authors present 2 main findings to support their claim. The first is that NIM811, an mPTP inhibitor, presents an effect similar to postconditioning. This finding indisputably shows that mPTP opening is involved in reperfusion injury. The results of NIM811 and postconditioning were both partial, however, and possible additive effects of both treatments were not determined. As a result, these experiments do not exclude that postconditioning can act on a pathway independent of mPTP opening. The second finding the authors present is an experiment with isolated mitochondria, which indicates that larger Ca2+ loads are required to induce Ca2+ release in …
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