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BACKGROUND Hypothermic cardioplegia provides myocellular protection, yet postischemic dysfunction remains a significant problem. Interestingly, the subcellular changes in hibernation parallel the altered biology of induced cardiac ischemia but are well tolerated by hibernated mammalian myocardium. An uncharacterized factor derived from hibernating animals, hibernation induction trigger (HIT), has been shown to induce hibernation in active animals and afford myocardial protection after ischemia-reperfusion injury. Therefore, it was of interest to further characterize the cardioprotective effects of HIT in the setting of ischemia-reperfusion injury. RESULTS To determine whether HIT could improve myocardial recovery after global ischemia, isolated rabbit hearts received either standard cardioplegia or HIT in the cardioplegia or underwent preperfusion with HIT before cardioplegia. Alternatively, to determine whether HIT requires metabolic alteration, additional rabbits had in vivo pretreatment with HIT from 15 minutes to 5 days before ischemia. All hearts underwent 2 hours of global ischemia at 34 degrees C. Recovery of postischemic isovolumic developed pressure, coronary flows, and MVO2 were compared. Compared with vehicle pretreatment, HIT pretreatment (1 hour) significantly enhanced indexes of functional recovery, including developed pressure (38 +/- 3 versus 69 +/- 7 mm Hg) and coronary flow (46 +/- 2 versus 82 +/- 11 mL/min). In addition, ultrastructural morphology was preserved but only with in vivo pretreatment. Liver protein content was not increased in rabbits treated from 12 hours to 5 days with HIT versus controls, belying a protein neosynthesis mechanism. However, the temporal sequences suggested conversion of an inactive HIT profactor to an active form. CONCLUSIONS Administration of serum derived from hibernating black bears to rabbits affords protection against ischemia-reperfusion injury compared with vehicle (saline)-treated animals in a rabbit isolated heart preparation. It is apparent that HIT deserves further identification and mechanistic study in the setting of ischemia-reperfusion injury.
S F Bolling, and
M B Benedict, and
N L Tramontini, and
K S Kilgore, and
H H Harlow, and
T P Su, and
P R Oeltgen
September 1997,
The Annals of thoracic surgery,
S F Bolling, and
M B Benedict, and
N L Tramontini, and
K S Kilgore, and
H H Harlow, and
T P Su, and
P R Oeltgen
March 2015,
Basic research in cardiology,
S F Bolling, and
M B Benedict, and
N L Tramontini, and
K S Kilgore, and
H H Harlow, and
T P Su, and
P R Oeltgen
January 1997,
European heart journal,
S F Bolling, and
M B Benedict, and
N L Tramontini, and
K S Kilgore, and
H H Harlow, and
T P Su, and
P R Oeltgen
December 1997,
Comparative biochemistry and physiology. Part A, Physiology,
S F Bolling, and
M B Benedict, and
N L Tramontini, and
K S Kilgore, and
H H Harlow, and
T P Su, and
P R Oeltgen
June 2003,
Circulation research,
S F Bolling, and
M B Benedict, and
N L Tramontini, and
K S Kilgore, and
H H Harlow, and
T P Su, and
P R Oeltgen
January 1995,
British journal of hospital medicine,
S F Bolling, and
M B Benedict, and
N L Tramontini, and
K S Kilgore, and
H H Harlow, and
T P Su, and
P R Oeltgen
January 1995,
Basic research in cardiology,
S F Bolling, and
M B Benedict, and
N L Tramontini, and
K S Kilgore, and
H H Harlow, and
T P Su, and
P R Oeltgen
May 2002,
Italian heart journal : official journal of the Italian Federation of Cardiology,
S F Bolling, and
M B Benedict, and
N L Tramontini, and
K S Kilgore, and
H H Harlow, and
T P Su, and
P R Oeltgen
September 1992,
Lancet (London, England),
S F Bolling, and
M B Benedict, and
N L Tramontini, and
K S Kilgore, and
H H Harlow, and
T P Su, and
P R Oeltgen
June 1992,
South African journal of surgery. Suid-Afrikaanse tydskrif vir chirurgie,
