Ina Lackner1, Birte Weber1, Deborah Knecht1, Klemens Horst2, Borna Relja3, Florian Gebhard1, Hans-Christoph Pape4, Markus Huber-Lang5, Frank Hildebrand2, Miriam Kalbitz1. 1. Department of Traumatology, Hand-, Plastic-, and Reconstructive Surgery, Center of Surgery, University of Ulm, Ulm, Germany. 2. Department of Orthopaedic Trauma, RWTH Aachen University, Aachen, Germany. 3. Department of Trauma-, Hand- and Reconstructive Surgery, University Hospital Frankfurt, Goethe University, Frankfurt/Main, Germany. 4. Department of Trauma Surgery, University Hospital Zurich, Zurich, Switzerland. 5. Institute of Clinical- and Experimental Trauma-Immunology, University of Ulm, Ulm, Germany.
Abstract
OBJECTIVE: The aim of this study was to define the influence of trauma on cardiac glucose and fatty acid transport. The effects were investigated in vivo in a porcine mono- and polytrauma model and in vitro in human cardiomyocytes, which were treated simultaneously with different inflammatory substances, mimicking posttraumatic inflammatory conditions. METHODS AND RESULTS: In the porcine fracture- and polytrauma model, blood glucose concentrations were measured by blood gas analysis during an observation period of 72 h. The expression of cardiac glucose and fatty acid transporters in the left ventricle was determined by RT-qPCR and immunofluorescence. Cardiac and hepatic glycogen storage was examined. Furthermore, human cardiomyocytes were exposed to a defined trauma-cocktail and the expression levels of glucose- and fatty acid transporters were determined. Early after polytrauma, hyperglycemia was observed. After 48 and 72 h, pigs with fracture- and polytrauma developed hypoglycemia. The propofol demand significantly increased posttrauma. The hepatic glycogen concentration was reduced 72 h after trauma. Cardiac glucose and fatty acid transporters changed in both trauma models in vivo as well as in vitro in human cardiomyocytes in presence of proinflammatory mediators. CONCLUSIONS: Monotrauma as well as polytrauma changed the cardiac energy transport by altering the expression of glucose and fatty acid transporters. In vitro data suggest that human cardiomyocytes shift to a state alike myocardial hibernation preferring glucose as primary energy source to maintain cardiac function.
OBJECTIVE: The aim of this study was to define the influence of trauma on cardiac glucose and fatty acid transport. The effects were investigated in vivo in a porcine mono- and polytrauma model and in vitro in human cardiomyocytes, which were treated simultaneously with different inflammatory substances, mimicking posttraumatic inflammatory conditions. METHODS AND RESULTS: In the porcine fracture- and polytrauma model, blood glucose concentrations were measured by blood gas analysis during an observation period of 72 h. The expression of cardiac glucose and fatty acid transporters in the left ventricle was determined by RT-qPCR and immunofluorescence. Cardiac and hepatic glycogen storage was examined. Furthermore, human cardiomyocytes were exposed to a defined trauma-cocktail and the expression levels of glucose- and fatty acid transporters were determined. Early after polytrauma, hyperglycemia was observed. After 48 and 72 h, pigs with fracture- and polytrauma developed hypoglycemia. The propofol demand significantly increased posttrauma. The hepatic glycogen concentration was reduced 72 h after trauma. Cardiac glucose and fatty acid transporters changed in both trauma models in vivo as well as in vitro in human cardiomyocytes in presence of proinflammatory mediators. CONCLUSIONS: Monotrauma as well as polytrauma changed the cardiac energy transport by altering the expression of glucose and fatty acid transporters. In vitro data suggest that human cardiomyocytes shift to a state alike myocardial hibernation preferring glucose as primary energy source to maintain cardiac function.
Authors: Henning Madry; Susanne Grässel; Ulrich Nöth; Borna Relja; Anke Bernstein; Denitsa Docheva; Max Daniel Kauther; Jan Christoph Katthagen; Rainer Bader; Martijn van Griensven; Dieter C Wirtz; Michael J Raschke; Markus Huber-Lang Journal: Eur J Med Res Date: 2021-06-14 Impact factor: 2.175