THE IMPACT OF CARDIAC ARREST ON REGIONAL CEREBRAL GLUCOSE METABOLISM IN RATS

Introduction Cardiac Arrest (CA) is the most important cause of global cerebral ischemia and despite wide efforts to improve the outcome, only a minority of resuscitated patients are discharged in good neurological condition. The physiopathological events occurring during and after brain ischemia are very complex and only partially understood. In this experimental animal study, in vivo PET and ex vivo autoradiography with [18F]FDG were used to evaluate the early cerebral glucose metabolism after cardiac arrest and resuscitation and how it is affected by desflurane anesthesia. Methods Adult rats (300-350 gr) were distributed into three groups: i) cardiac arrest group: rats underwent 8 minutes CA and resuscitation (n=10; 5% desflurane)[1]; ii) sham group: rats were subjected to the same surgical procedure of the first group (n=4; 5% desflurane); iii) control group: rats were used as baseline control of glucose uptake and performed only autoradiography study, without any anesthetic surgical procedure (n=4; no anesthesia). After surgery, CA and sham animals performed a 30 min [18F]FDG PET scan centered on head followed by autoradiography. ROI analysis was performed both on PET and on autoradiographic images. PET and autoradiography data were expressed as absolute uptake (%ID/gmax and %ID/mm2, respectively) and as relative uptake (specific area to mean brain activity ratio). Results Desflurane anesthesia decreased the absolute glucose uptake of about 70% in all brain areas (sham vs control, p<0.05). Post-ischemic rats showed a significant relative decrease (20-28%, p<0.01 in all cortices) in neocortical areas in comparison to sham group. The metabolism remained around sham's levels in hippocampus, striatum, and thalamus. Finally, resuscitated rats had an increased relative metabolism in midbrain (16%, p<0.0001), pons (16%, p<0.05), and cerebellum (24%, p<0.001). The same trend was observed in PET images. Conclusions PET imaging allowed to monitor changes in glucose metabolism after CA. We found a metabolic fingerprint characterizing the early recovery phase from global brain ischemia and each brain region showed a specific metabolic reaction to the ischemia. Decreased metabolism in cortical areas may be due to impairment in cellular bionergetic system, including glycolysis pathway. This model can be used to test new treatments for AC and to monitor also inflammation. References [1] M Haenggi et al, "Do different anesthesia regimes affect hippocampal apoptosis and neurologic deficits in a rodent cardiac arrest model?" BMC anesthesiology, in press