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Myocardial ischemic preconditioning and mitochondrial F1F0-ATPase activity

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Abstract

A short period of ischemia followed by reperfusion (ischemic preconditioning) is known to trigger mechanisms that contribute to the prevention of ATP depletion. In ischemic conditions, most of the ATP hydrolysis can be attributed to mitochondrial F1F0-ATPase (ATP synthase). The purpose of the present study was to examine the effect of myocardial ischemic preconditioning on the kinetics of ATP hydrolysis by F1F0-ATPase. Preconditioning was accomplished by three 3-min periods of global ischemia separated by 3 min of reperfusion. Steady state ATP hydrolysis rates in both control and preconditioned mitochondria were not significantly different. This suggests that a large influence of the enzyme on the preconditioning mechanism may be excluded. However, the time required by the reaction to reach the steady state rate was increased in the preconditioned group before sustained ischemia, and it was even more enhanced in the first 5 min of reperfusion (101 ± 3.0 sec in preconditioned vs. 83.4 ± 4.4 sec in controls, p ≶ 0.05). These results suggest that this transient increase in activation time may contribute to the cardioprotection by slowing the ATP depletion in the very critical early phase of post-ischemic reperfusion.

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Authors and Affiliations

  1. Section on Brain Physiology and Metabolism, National Institute of Aging, NIH Building 10, Room 6C103, 9000 Rockville Pike, Bethesda, MD, 20892, USA

    Francesca Bosetti

  2. Dipartimento di Scienze dell'Uomo e dell'Ambiente, Sezione di Chimica e Biochemica Medica, Università di Pisa, Italy

    Gongyuan Yu & Simonetta Ronca-Testoni

  3. Scuola Superiore di Studi Universitari e di Perfezionamento S. Anna, Via G. Carducci 40, 56127, Pisa, Italy

    Riccardo Zucchi & Giancarlo Solaini

Authors
  1. Francesca Bosetti
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  2. Gongyuan Yu
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  3. Riccardo Zucchi
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  4. Simonetta Ronca-Testoni
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  5. Giancarlo Solaini
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Bosetti, F., Yu, G., Zucchi, R. et al. Myocardial ischemic preconditioning and mitochondrial F1F0-ATPase activity. Mol Cell Biochem 215, 31–38 (2000). https://doi.org/10.1023/A:1026558922596

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