Premium
Hibernating mammals have enhanced survival and reduced gut damage after hemorrhage
Author(s) -
Carey Hannah V.,
Potter K. T.,
Peters T. L.,
Epperson L. E.,
Rose J. C.,
Martin S. L.
Publication year - 2006
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.20.5.a1382-a
Subject(s) - torpor , hibernation (computing) , biology , ischemia , medicine , endocrinology , pharmacology , thermoregulation , state (computer science) , algorithm , computer science
Torpor‐arousal cycles in hibernators involve marked changes in tissue perfusion that can compromise delivery of O 2 and nutrients to tissue beds. This stress is well‐tolerated by hibernators, due to metabolic depression that reduces O 2 demand and possibly to other protective mechanisms associated with the hibernation phenotype. We showed previously that hibernation in ground squirrels (GS) provides protection from cold ischemia‐reperfusion injury in liver. Here we examined whether GS have enhanced survival and reduced tissue damage after massive hemorrhage compared with non‐hibernating species. A non‐survival, anesthetized model of 60% blood loss was used in rats and 13‐lined GS. All rats died within 70 min post hemorrhage (mean survival time = 33 ± 1 min, n=5). Survival time was at least 12‐fold greater in hibernating or pre‐hibernation GS (393 ± 45 min, n=4; experiments were terminated before death in 3 of the 4 GS). Gut mucosa showed significant histological damage in all rats after hemorrhage, with minimal effects in GS. Proteomic approaches are being used to identify candidate molecules in GS that may be responsible for hibernation‐induced protection. Potential candidates include proteins involved in detoxification and antioxidant defense and chaperone proteins associated with the unfolded protein response. Understanding the natural biochemistry of stress resistance in hibernators will allow for mimicking its features in human medicine. Supported by DARPA W81XWH‐05‐02‐0016 (Approved for Public Release, Distribution Unlimited).