Abstract
1. Langendorff-perfusion of rat hearts with either 10 mM caffeine or 1 mM 2,4-dinitrophenol (DNP) caused severe ultrastructural damage to the myofilaments and mitochondria that was similar to that found in a standard Ca 2+-paradox. 2. This damage occurred in the presence and absence of extracellular Ca 2+ 3. Creatine kinase (CK) release (indicative of sarcolemma breakdown) was not recorded unless the caffeine- or DNP-perfusion was preceded by Ca 2+ 0-depletion. 4. It is concluded that: (i) the pathways leading to damage to the myofilaments and sarcolemma are independent; (ii) the CK release mechanism requires dual activation of Ca 2+ 0-depletion plus a rise in [Ca 2+] i; and (iii) current theories concerning the mechanisms underlying the genesis of the Ca 2+-paradox are incorrect or incomplete.
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