Preconditioning with Sub-lethal Ischemia or Normobaric Hyperoxia Reduce Brain Edema in the Rat

Recent studies suggest that sub-lethal ischemia protect the brain from subsequent ischemic injury. In this, we sought to identify and clarify the nature of changes in the blood brain barrier permeability and brain edema. Rats were divided into five experimental main groups, each of 35 animals. The first group was exposed to normobaric hyperoxia (HO; 95% oxygen) for 4 continuous hours of each day for each of 6 consecutive days and subjected to 60 min middle cerebral artery occlusion (MCAO) in seventh day. The second group acted as controls, and was not received any surgery except 60 min middle cerebral artery occlusion in seventh day. The third group acted as a model of ischemic preconditioning was subjected to 10 min of temporary middle cerebral artery occlusion (tMCAO) in sixth day and subjected to 60 min middle cerebral artery occlusion (MCAO) in seventh day. The fourth group acted as shams, and was subjected to surgery with 10 min temporary middle cerebral artery occlusion in the sixth day. The fifth group acted as intact, and was not subjected to any surgery (without reperfusion; WOR). Last four groups were exposed to normobaric normoxia (the 21% oxygen in room air [RA]) according to the same protocol. Each main group subdivided into three subgroups (n=7) for assessment of infarct volume, blood brain barrier permeability, and brain edema. After 24 hours, neurologic deficit score (NDS), infarct volume, blood brain barrier permeability, and brain edema were assessed in subgroups. Preconditioning with tMCAO and HO decreased NDS and infarct volume, brain barrier permeability, and brain edema. tMCAO are associated with neurologic deficit scores, infarct volume, blood brain barrier permeability, and brain edema, consistent with an active role in the genesis of ischemic protection.

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