Journal
CRITICAL CARE MEDICINE
Volume 33, Issue 12, Pages 2752-2756Publisher
LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1097/01.CCM.0000189943.60945.77
Keywords
sepsis; myocardial hibernation; myocardium; heart; glucose utilization; glycogen; glucose transporters; GLUT4
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Funding
- NIGMS NIH HHS [R01GM 59930] Funding Source: Medline
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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. Design: Prospective observational study aimed at identifying the characteristic changes of hibernation in the septic heart. Setting: University hospital-based laboratory. Subjects: Forty-three C57BI6 male mice. Interventions: Mice underwent cecal ligation and double puncture, sham operation, or no operation and were evaluated 48 hrs after the procedure. Measurements and Main 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.
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