Inhibition of myocardial injury by ischemic postconditioning during reperfusion: comparison with ischemic preconditioning.
By Zhi-Qing Zhao, J. Corvera, Michael E. Halkos, Faraz Kerendi, Ningping Wang, R. Guyton, J. Vinten-johansen. American Journal of Physiology. Heart and Circulatory Physiology, 2003
2,224 citations recorded by the source corpus.
Subfields: Developmental Neuroscience, Emergency Medicine, Pathology and Forensic Medicine
View Paper: https://www.semanticscholar.org/paper/c8e2ba8254c15f1ca42c3d86fc19d89d14f55573
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Citations in the corpus
- Postconditioning attenuates myocardial ischemia-reperfusion injury by inhibiting events in the early minutes of reperfusion. (2004, background): “[9,10] in the canine model, and suggest that at least the later phase of ROS generation is attenuated by postconditioning.”
- Mechanisms underlying acute protection from cardiac ischemia-reperfusion injury. (2008, background): “In 2003 Zhao et al. reported that intermittent reperfusion, after ischemia, can also reduce infarct size (287).”
- Myocardial ischemia-reperfusion injury: a neglected therapeutic target. (2013, positive): “In contrast to unimpeded reperfusion, IPost is intermittent reperfusion of the acute ischemic myocardium, which has been reported to prevent myocardial reperfusion injury and reduce MI size by 40%–50% (61).”
- Postconditioning: A Form of “Modified Reperfusion” Protects the Myocardium by Activating the Phosphatidylinositol 3-Kinase–Akt Pathway (2004, methodology): “02% dimethyl sulfoxide (DMSO) vehicle (n 4) for the first 15 minutes of reperfusion; (2) IPC (n 11), comprising 2 cycles of 5 minutes of global ischemia followed by 10 minutes of reperfusion before the index ischemia; (3) Postcond (n 10), comprising 6 cycles of 10 seconds of reperfusion followed by ”