Abstract
The effect of lidocaine (2 mM) on cell damage in the perfused rat heart is compared in three experimental protocols: the Ca(2+)-paradox, the O2-paradox and perfusion with caffeine. Lidocaine protected against creatine kinase (CK) release when perfused throughout or only during the priming stage in all three protocols. Lidocaine also protects against CK release in the Ca(2+)-paradox when present only during Ca(2+)-reperfusion. Lidocaine protects against myofilament damage in the Ca(2+)-paradox but not in the O2-paradox and caffeine protocols, even though CK release is inhibited. Analysis of these different effects of lidocaine on the priming and full activation stages in the three protocols suggests the sequence of the underlying biochemical events of the two separate damage pathways associated with the release of cytosolic proteins and the degradation of the myofilament apparatus.
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