Increased intracellular Ca2+ and SR Ca2+ load contribute to arrhythmias after acidosis in rat heart. Role of Ca2+/calmodulin-dependent protein kinase II.

@article{Said2008IncreasedIC,
  title={Increased intracellular Ca2+ and SR Ca2+ load contribute to arrhythmias after acidosis in rat heart. Role of Ca2+/calmodulin-dependent protein kinase II.},
  author={M. Bakheit Said and Romina V. Becerra and Julieta Palomeque and Gustavo Juan Rinaldi and Marcia A. Kaetzel and Paula L. Diaz-Sylvester and Julio A. Copello and John R. Dedman and Cecilia Mundi{\~n}a-Weilenmann and Leticia Vittone and Alicia R. Mattiazzi},
  journal={American journal of physiology. Heart and circulatory physiology},
  year={2008},
  volume={295 4},
  pages={H1669-83}
}
Returning to normal pH after acidosis, similar to reperfusion after ischemia, is prone to arrhythmias. The type and mechanisms of these arrhythmias have never been explored and were the aim of the present work. Langendorff-perfused rat/mice hearts and rat-isolated myocytes were subjected to respiratory acidosis and then returned to normal pH. Monophasic action potentials and left ventricular developed pressure were recorded. The removal of acidosis provoked ectopic beats that were blunted by 1… CONTINUE READING

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Experiments in planar lipid bilayers confirmed the reversible inhibitory effect of acidosis on RyR2 .
Experiments in planar lipid bilayers confirmed the reversible inhibitory effect of acidosis on RyR2 .
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