Induction of short ischemic episodes after the stroke can be neuroprotective. Hypoxia was also suggested as the factor producing neuroprotection in the animal brain. Therefore in our studies we aimed to test if normobaric hypoxia (10% of oxygen) induced after ischemia could prevent neuronal loss. The model of hypoxia-ischemia (H-I) in 7-days old rats and the model of global forebrain ischemia in Mongolian gerbils were used. 7-days old rats were subjected to H-I and the first of three episodes of postconditioning hypoxia was induced 1, 3 or 6 hours after H-I episode. After ischemia gerbils were subjected to three trials of 1h hypoxia applied every 24 hours. The first episode was induced immediately, 2.5 h or 6 h after the ischemic insult. The morphological and behavioral effects of the postconditioning were evaluated. In the model of H-I on rats, the assessment of brain mass deficit revealed that normobaric hypoxia induced signifficant neuroprotection when applied 1 h or 6 h after H-I but not 2.5 h. In the global forebrain ischemia model normobaric hypoxia itself was harmless and the number of pyramidal neurons evaluated in CA1 region was the same as in the sham group. The neuroprotective effect of normobaric hypoxia postconditioning was observed when hypoxia was induced immediately after ischemia but not 2.5 or 6 hours after the insult. The behavioral evaluation showed only small improvement in nest-building test in postconditioned animals. Presented data show that normobaric hypoxia postconditioning produces the neuroprotective effect, however the therapeutic window of this treatment varies according to the model of brain ischemia. Supported by MSHE grant NN401003935.
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