Alessandro Putzu1,2, Silvia Valtorta3,4, Giuseppe Di Grigoli3,5, Matthias Haenggi6, Sara Belloli3,5, Antonio Malgaroli7, Marco Gemma1,2, Giovanni Landoni1,2, Luigi Beretta1,2, Rosa Maria Moresco8,9. 1. Department of Anesthesia and Intensive Care, IRCCS San Raffaele Scientific Institute, Milan, Italy. 2. Vita-Salute San Raffaele University, Milan, Italy. 3. Experimental Imaging Center, IRCCS San Raffaele Scientific Institute, Milan, Italy. 4. Department of Medicine and Surgery, University of Milano-Bicocca, Via Cadore 48, 20900, Monza, MB, Italy. 5. IBFM-CNR, Milan, Italy. 6. Department of Intensive Care Medicine, Inselspital, Bern University Hospital, University of Bern, Bern, Switzerland. 7. Neurobiology of Learning Unit, Division of Neuroscience, Vita-Salute San Raffaele University, Milan, Italy. 8. Experimental Imaging Center, IRCCS San Raffaele Scientific Institute, Milan, Italy. moresco.rosamaria@hsr.it. 9. Department of Medicine and Surgery, University of Milano-Bicocca, Via Cadore 48, 20900, Monza, MB, Italy. moresco.rosamaria@hsr.it.
Abstract
BACKGROUND: Cardiac arrest is an important cause of morbidity and mortality. Brain injury severity and prognosis of cardiac arrest patients are related to the cerebral areas affected. To this aim, we evaluated the variability and the distribution of brain glucose metabolism after cardiac arrest and resuscitation in an adult rat model. METHODS: Ten rats underwent 8-min cardiac arrest, induced with a mixture of potassium and esmolol, and resuscitation, performed with chest compressions and epinephrine. Eight sham animals received anesthesia and experimental procedures identical to the ischemic group except cardiac arrest induction. Brain metabolism was assessed using [18F]FDG autoradiography and small animal-dedicated positron emission tomography. RESULTS: The absolute glucose metabolism measured with [18F]FDG autoradiography 2 h after cardiac arrest and resuscitation was lower in the frontal, parietal, occipital, and temporal cortices of cardiac arrest animals, showing, respectively, a 36% (p = 0.006), 32% (p = 0.016), 36% (p = 0.009), and 32% (p = 0.013) decrease compared to sham group. Striatum, hippocampus, thalamus, brainstem, and cerebellum showed no significant changes. Relative regional metabolism indicated a redistribution of metabolism from cortical area to brainstem and cerebellum. CONCLUSIONS: Our data suggest that cerebral regions have different susceptibility to moderate global ischemia in terms of glucose metabolism. The neocortex showed a higher sensibility to hypoxia-ischemia than other regions. Other subcortical regions, in particular brainstem and cerebellum, showed no significant change compared to non-ischemic rats.
BACKGROUND:Cardiac arrest is an important cause of morbidity and mortality. Brain injury severity and prognosis of cardiac arrestpatients are related to the cerebral areas affected. To this aim, we evaluated the variability and the distribution of brain glucose metabolism after cardiac arrest and resuscitation in an adult rat model. METHODS: Ten rats underwent 8-min cardiac arrest, induced with a mixture of potassium and esmolol, and resuscitation, performed with chest compressions and epinephrine. Eight sham animals received anesthesia and experimental procedures identical to the ischemic group except cardiac arrest induction. Brain metabolism was assessed using [18F]FDG autoradiography and small animal-dedicated positron emission tomography. RESULTS: The absolute glucose metabolism measured with [18F]FDG autoradiography 2 h after cardiac arrest and resuscitation was lower in the frontal, parietal, occipital, and temporal cortices of cardiac arrest animals, showing, respectively, a 36% (p = 0.006), 32% (p = 0.016), 36% (p = 0.009), and 32% (p = 0.013) decrease compared to sham group. Striatum, hippocampus, thalamus, brainstem, and cerebellum showed no significant changes. Relative regional metabolism indicated a redistribution of metabolism from cortical area to brainstem and cerebellum. CONCLUSIONS: Our data suggest that cerebral regions have different susceptibility to moderate global ischemia in terms of glucose metabolism. The neocortex showed a higher sensibility to hypoxia-ischemia than other regions. Other subcortical regions, in particular brainstem and cerebellum, showed no significant change compared to non-ischemicrats.
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