On completion of this article, the reader should be able to:
- Define myocardial hibernation.
- Explain physiologic changes in hibernating hearts.
- Use this information in a clinical setting.
Dr. Ferrari has disclosed that he is/was the recipient of direct grant/research funds from Novartis and GlaxoSmithKline. All of the remaining authors have disclosed that they have no financial relationships or interests in any commercial companies pertaining to this educational activity.
Wolters Kluwer Health has identified and resolved all faculty conflicts of interest regarding this educational activity.
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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.
Prospective observational study aimed at identifying the characteristic changes of hibernation in the septic heart.
University hospital-based laboratory.
Forty-three C57Bl6 male mice.
Mice underwent cecal ligation and double puncture, sham operation, or no operation and were evaluated 48 hrs after the procedure.
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.
Sepsis-associated cardiac dysfunction may reflect hibernation. Furthermore, such down-regulation of cellular function may underlie sepsis-induced dysfunction in other organ systems.
Assistant Professor of Anesthesiology and Pediatrics (RJL), Research Assistant (DAP), The Children’s Hospital of Philadelphia; Associate Professor, Director, Molecular Imaging Physics, Department of Radiology, Thomas Jefferson University (PDA); Assistant Professor (RZ), Professor Radiology and Physics (JSK), University of Pennsylvania; Associate Professor of Medicine, University of Pennsylvania School of Medicine, Associate Director, Noninvasive Imaging Laboratory, Hospital of the University of Pennsylvania (VAF); Professor of Anesthesia and Surgery, Department of Anesthesiology and Critical Care, University of Pennsylvania School of Medicine (CSD), Philadelphia, PA.
Supported, in part, by grant NIGMS R01GM 59930 from the National Institutes of Health (CSD).
The authors have no financial interests to disclose.