title: Hibernation induction trigger reduces hypoxic damage of swine skeletal muscle.
abstract: A link between the cardioprotective benefits of pharmacological preconditioning and natural mammalian hibernation is considered to involve the cellular activation of opioid receptors and subsequent opening of K(ATP) channels. In previous studies, we have demonstrated the protective effects of specific delta-opioid agonists against porcine cardiac ischemia/reperfusion injury. We hypothesize here that preincubation with hibernation induction trigger (HIT) should confer a similar protection in skeletal muscles. Therefore, muscle bundles from swine were pretreated with plasma from hibernating woodchucks (HWP) for 30 min, then exposed to hypoxia for 90 min and reoxygenation for 120 min. Stimulated twitch forces were assessed. The functional effects of pretreatment with nonhibernation (summer) woodchuck plasma, a K(ATP) blocker, or opioid antagonist were also studied. During the reoxygenation period, significantly greater force recoveries were observed only for bundles pretreated with HWP; this response was blocked by naloxone (P < 0.05). We conclude that HIT pretreatment could be used to confer protection against hypoxia/reperfusion injury of skeletal muscles of nonhibernators; it could potentially be utilized to prevent injury during surgical procedures requiring ischemia.
authors.affiliation: Department of Biomedical Engineering, University of Minnesota, Minneapolis, Minnesota, USA.
authors.forename: Jinback
authors.initials: J
authors.lastname: Hong
authors.forename: Daniel C
authors.initials: DC
authors.lastname: Sigg
authors.forename: James A
authors.initials: JA
authors.lastname: Coles
authors.forename: Peter R
authors.initials: PR
authors.lastname: Oeltgen
authors.forename: Henry J
authors.initials: HJ
authors.lastname: Harlow
authors.forename: Charles L
authors.initials: CL
authors.lastname: Soule
authors.forename: Paul A
authors.initials: PA
authors.lastname: Iaizzo
mesh_terms: D000818:Animals; D001798:Blood Proteins / Q000378:metabolism / Q000494:pharmacology; D006605:Hibernation / Q000502:physiology*; D000860:Hypoxia / Q000188:drug therapy* / Q000503:physiopathology / Q000517:prevention & control; D019194:Ischemic Preconditioning / Q000379:methods*; D008392:Marmota / Q000502:physiology; D008928:Mitochondria / Q000187:drug effects / Q000378:metabolism; D009119:Muscle Contraction / Q000187:drug effects / Q000502:physiology; D018763:Muscle Fatigue / Q000187:drug effects / Q000502:physiology; D018482:Muscle, Skeletal / Q000187:drug effects* / Q000378:metabolism / Q000503:physiopathology; D009292:Narcotic Antagonists / Q000494:pharmacology; D010455:Peptides; D026902:Potassium Channel Blockers / Q000494:pharmacology; D015221:Potassium Channels / Q000187:drug effects / Q000378:metabolism; D011506:Proteins / Q000378:metabolism / Q000494:pharmacology*; D011957:Receptors, Opioid / Q000187:drug effects / Q000378:metabolism; D020127:Recovery of Function / Q000187:drug effects / Q000502:physiology; D015427:Reperfusion Injury / Q000188:drug therapy* / Q000503:physiopathology / Q000517:prevention & control; D012621:Seasons; D034421:Sus scrofa
chemical_list: D001798:Blood Proteins; D009292:Narcotic Antagonists; D010455:Peptides; D026902:Potassium Channel Blockers; D015221:Potassium Channels; D011506:Proteins; D011957:Receptors, Opioid; C036932:hibernation induction trigger