Prolonged and Intermittent Bilateral Common Carotid Artery Occlusion Induces Brain Lipidome Changes in a Rat Stroke Model

Background: Recent studies suggest that prolonged and intermittent bilateral common carotid artery occlusion (prolonged bilateral common carotid artery occlusion (PO) and intermittent bilateral common carotid artery occlusion, respectively) can lead to reduced ischemia brain injury in ischemic tolerance. Objectives: In this study, we aimed to investigate the changes in brain lipidomics following prolonged and intermittent ischemic preconditioning. Materials andMethods: Two groups underwent bilateral common carotid artery occlusion either intermittently (for 3 continuous periods within a timeframe of 20 minutes, releasing 3 consecutive times, yielding a total of 9 minutes (intermittent bilateral common carotid artery occlusion)) or for 9 minutes continuously (prolonged bilateral common carotid artery occlusion). The third and fourth groups were used as control and sham (without ischemia) groups, respectively. The first three groups were subdivided into middle cerebral artery occlusion-operated (middle cerebral artery occlusion MCAO), for 60 minutes of ischemia) and intact (without any surgery) subgroups. After 1 hour of ischemia and 24 hours of reperfusion, the neurologic deficit score (neurological deficit score (NDS)) and the infarct volume (infarct volume) were assessed in the middle cerebral artery occlusion-operated subgroup. Brain lipidomics were measured in the intact subgroup and the sham group. Results: Preconditioning with prolonged bilateral common carotid artery occlusion and intermittent bilateral common carotid artery occlusion significantly decreased the neurological deficit scores and infarct volume and increased the levels of phosphatidylethanolamine, sphingomyelin, cholesterol ester, cholesterol, phosphatidylcholine, and cerebroside in the brain compared with the control and sham groups. Prolonged bilateral common carotid artery occlusion and intermittent bilateral common carotid artery occlusion significantly decreased the brain ceramide and lysophosphatidylcholine levels. The triglyceride levels in both groups (intermittent bilateral common carotid artery occlusion and prolonged bilateral common carotid artery occlusion) did not change in comparison with the control and sham groups. Conclusions: Although it seems that further studies are needed to clarify the real mechanisms of ischemic tolerance, ischemic preconditioning could decrease brain ischemia injury via changes in brain lipidomics.