What is it about?
Hibernating animals are resistant to either low temperature-induced irregular heartbeats (cardiac arrhythmias). However, their resistance to ischemia-induced arrhythmias during hibernating season is not known. Our goal was to investigate susceptibility to arrhythmias during coronary artery occlusion (CAO) in woodchucks in winter during hibernation season, in comparison to that in the summer. We have found that the heart of a hibernating animal in winter is more resistant to ischemia-induced arrhythmias and sudden cardiac death than in summer. We have also demonstrated that the susceptibility to oxidative stress-induced early afterdepolarizations (EADs) and triggered activities (TAs) is modified in hibernating mammalian hearts during winter. The mechanism may involve increase antioxidative stress ability and subsequently decreased Ca2+/calmodulin-dependent protein kinase II activity, which therefore confers resistance against oxidative stress-induced EADs and TAs. Adenoviarl vector-mediated overexpression of catalase or inhibition of CaMKII may confer the transition of the woodchuck heart from a less protective "summer mode" to a higher protective "winter mode". The profound protection conferred may provide insights into clinical directions for therapy of arrhythmias. Manipulation of oxidative stress and CaMKII signaling may hold therapeutic potential for treating cardiac arrhythmias.
The following have contributed to this page: Lai-Hua Xie
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