Hypoxic postconditioning reduces cardiomyocyte loss by inhibiting ROS generation and intracellular Ca2+ overload.

@article{Sun2005HypoxicPR,
  title={Hypoxic postconditioning reduces cardiomyocyte loss by inhibiting ROS generation and intracellular Ca2+ overload.},
  author={He-Ying Sun and N Wang and Faraz Kerendi and Michael E. Halkos and Hajime Kin and Robert A. Guyton and Jakob Vinten-Johansen and Zhi-qing Zhao},
  journal={American journal of physiology. Heart and circulatory physiology},
  year={2005},
  volume={288 4},
  pages={H1900-8}
}
We have shown that intermittent interruption of immediate reflow at reperfusion (i.e., postconditioning) reduces infarct size in in vivo models after ischemia. Cardioprotection of postconditioning has been associated with attenuation of neutrophil-related events. However, it is unknown whether postconditioning before reoxygenation after hypoxia in cultured cardiomyocytes in the absence of neutrophils confers protection. This study tested the hypothesis that prevention of cardiomyocyte damage by… CONTINUE READING
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