Postconditioning attenuates myocardial ischemia-reperfusion injury by inhibiting events in the early minutes of reperfusion.
By H. Kin, Zhi-Qing Zhao, He-ying Sun, Ningping Wang, J. Corvera, Michael E. Halkos, Faraz Kerendi, R. Guyton, J. Vinten-johansen. Cardiovascular Research, 2004
606 citations recorded by the source corpus.
Subfields: Cardiology and Cardiovascular Medicine, Pathology and Forensic Medicine, Surgery
View Paper: https://www.semanticscholar.org/paper/11816d84eb7c9043c62229c6db45c81163a0b206
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In Cardiology and Cardiovascular Medicine
In Pathology and Forensic Medicine
Citations in the corpus
- Interaction of Cardiovascular Risk Factors with Myocardial Ischemia/Reperfusion Injury, Preconditioning, and Postconditioning (2007, background): “…2006a; Schwartz and Lagranha, 2006), but once protection is achieved increasing the number of postconditioning ischemia/ reperfusion episodes does not further decrease infarct size in isolated rat hearts (Tsang et al., 2004) and in rats (Kin et al., 2004) and rabbits (Yang et al., 2004) in vivo.”
- 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 ”
- Multitarget Strategies to Reduce Myocardial Ischemia/Reperfusion Injury: JACC Review Topic of the Week. (2019, background): “The endogenous cardioprotective strategies of IPC, IPost, and RIC are known to protect the heart through a number of different signaling pathways and might therefore be assumed to confer a stronger cardioprotective effect than a single-target agent.”