Could hibernators hold the key to improving organ preservation?

m cold storage followed by warm reperfusion. Studies by other scientists have shown that this can lead to the release of potentially damaging chemicals, such as reactive oxygen species and pro-inflammatory cytokines that can produce oxidative stress. In contrast, there is little evidence of activation of Kupffer cells in hibernator livers after long-term cold storage, an effect that should reduce liver damage. Hibernator livers also maintain gluthathione redox balance to a better degree than do rats with increasing cold storage time. Because glutathione is an antioxidant, this is another mechanism by which hibernator organs may be protected from cold ischemia/reperfusion injury.

  • A transcription factor, NF-kB, which can initiate pro-inflammatory pathways and has been implicated in liver injury after cold storage/reperfusion, is activated in rat livers. This occurs after 24 hours of cold storage in rat livers, but it is not activated in livers of hibernators.

  • Hibernators have much higher levels of a protective protein (known as HSP70) in their livers than do rats. HSP70 has been shown in other studies to confer protection to tissues and organs when they are stressed, such as after cold storage and reperfusion.


    Taken together, the current and earlier studies provide exciting new directions that will help researchers identify the specific mechanisms that hibernators use to avoid tissue and organ damage during the highly altered physiology that accompanies hibernation. By fully understanding these mechanisms, these researchers believe that therapeutic advances can be developed which will protect human organs during trauma states and organ transplantation.


  • Contact: Donna Krupa
    American Physiological Society

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