Changes in the Severity of Hypoxic Brain Damage in Rats Due to Hypoxic Postconditioning

Abstract

The aim of the present work was to assess the neuroprotective action of postconditioning (PostC) with moderate hypobaric hypoxia (360 mmHg, 2 h) in a model of severe hypoxic brain damage (180 mmHg, 3 h). PostC consisted of three sessions of moderate hypoxia with 24-h intervals using two schemes – PostC was started 3 h (early PostC) or 24 h (late PostC) after severe hypoxia. Histological methods and automated image analysis were used to assess the extent of neuron damage in the hippocampus and neocortex seven days after severe hypoxia. Severe hypoxia led to death of 24% of neurons in layer V of the neocortex, 26% of neurons in hippocampal field CA1, and 22% of neurons in hippocampal field CA4. Early PostC prevented neuron death in field CA1 and significantly decreased the number of dead cells in field CA4 (to 10%) and the neocortex (to 13%). Delayed PostC completely prevented neuron damage in hippocampal field CA4 and the neocortex and significantly but not completely in field CA1 (12% of neurons died). These results provide evidence that PostC with moderate hypobaric hypoxia had neuroprotective effects, decreasing the extent of damage to susceptible brain formations (the hippocampus and neocortex); the efficacy of neuroprotection depended on the timing of the first session of PostC.