title: Evidence of myocardial hibernation in the septic heart.
abstract: OBJECTIVE
  Myocardial hibernation is an adaptive response to ischemia and hypoxia. Hibernating cardiomyocytes are reversibly hypocontractile and demonstrate characteristic metabolic and ultrastructural changes. These include a switch in primary substrate utilization from fatty acids to glucose, up-regulation of the myocardial specific glucose transporters (GLUT1 and GLUT4), and glycogen deposition within and between cardiomyocytes. We hypothesized that myocardial hibernation may underlie sepsis-associated myocardial depression.
  
  
  METHODS
  Prospective observational study aimed at identifying the characteristic changes of hibernation in the septic heart.
  
  
  METHODS
  University hospital-based laboratory.
  
  
  METHODS
  Forty-three C57Bl6 male mice.
  
  
  METHODS
  Mice underwent cecal ligation and double puncture, sham operation, or no operation and were evaluated 48 hrs after the procedure.
  
  
  RESULTS
  Using novel, clinically relevant technology such as magnetic resonance imaging, positron emission tomography, and single photon emission computed tomography imaging, we found septic mice to have diminished cardiac performance, increased myocardial glucose uptake, increased steady-state levels of myocardial GLUT4, and increased deposits of glycogen, recapitulating the changes during hibernation. Importantly, these changes occurred in the setting of preserved arterial oxygen tension and myocardial perfusion.
  
  
  CONCLUSIONS
  Sepsis-associated cardiac dysfunction may reflect hibernation. Furthermore, such down-regulation of cellular function may underlie sepsis-induced dysfunction in other organ systems.
authors.affiliation: The Children's Hospital of Philadelphia, Philadelphia, PA, USA.
authors.forename: Richard J
authors.initials: RJ
authors.lastname: Levy
authors.forename: David A
authors.initials: DA
authors.lastname: Piel
authors.forename: Paul D
authors.initials: PD
authors.lastname: Acton
authors.forename: Rong
authors.initials: R
authors.lastname: Zhou
authors.forename: Victor A
authors.initials: VA
authors.lastname: Ferrari
authors.forename: Joel S
authors.initials: JS
authors.lastname: Karp
authors.forename: Clifford S
authors.initials: CS
authors.lastname: Deutschman
mesh_terms: D000818:Animals; D001786:Blood Glucose / Q000378:metabolism; D004734:Energy Metabolism / Q000502:physiology; D005227:Fatty Acids / Q000378:metabolism; D051272:Glucose Transporter Type 1 / Q000502:physiology; D051275:Glucose Transporter Type 4 / Q000502:physiology; D006003:Glycogen / Q000378:metabolism; D006439:Hemodynamics / Q000502:physiology; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D009200:Myocardial Contraction / Q000502:physiology; D017682:Myocardial Stunning / Q000473:pathology / Q000503:physiopathology*; D032383:Myocytes, Cardiac / Q000473:pathology / Q000502:physiology*; D012772:Shock, Septic / Q000473:pathology / Q000503:physiopathology*; D015854:Up-Regulation / Q000502:physiology
chemical_list: D001786:Blood Glucose; D005227:Fatty Acids; D051272:Glucose Transporter Type 1; D051275:Glucose Transporter Type 4; C495678:Slc2a1 protein, mouse; C495693:Slc2a4 protein, mouse; D006003:Glycogen