Vorob'ev M G, Rybnikov E A, Samoĭlov M O
Morfologiia. 2012;141(1):12-5.
The present study has been aimed to estimate a neuroprotective effect of postconditioning (PostC) by using mild hypobaric hypoxia (360 mm Hg, 2 h) in a model of severe hypoxic brain injury (180 mm Hg, 3 h) in rats. PostC was performed by three trials of mild hypoxia with 24 h intervals, according to two different protocols--PostC was started 3 h (early PostC) or 24 h (delayed PostC) following severe hypoxia. Using histological methods and computer image analysis, loss of neurons in hippocampus and neocortex was analyzed 7 days after severe hypoxia. Severe hypoxia caused loss of 24% of neurons in layer V of the neocortex, 26% of neurons in CA1 region of hippocampus and 22% of neurons in CA4 region. Early PostC prevented loss of neurons in CA1 region of hippocampus and significantly reduced loss of neurons in neocortex (to 13%) and in CA4 region (to 10%). Delayed PostC fully prevented neuronal damage in CA4 region of hippocampus and neocortex and was to a large extent but not completely protective in CA1 region (12% of neurons were lost). The results show that PostC performed by hypobaric hypoxia has a pronounced neuroprotective effect, reducing the loss of neurons in vulnerable structures of brain (hippocampus and neocortex). The efficacy of neuroprotection depends upon the time of presentation of the first PostC session.
本研究旨在通过在大鼠严重缺氧性脑损伤模型（180毫米汞柱，3小时）中使用轻度低压缺氧（360毫米汞柱，2小时）来评估后处理（PostC）的神经保护作用。根据两种不同方案，后处理通过三次间隔24小时的轻度缺氧试验进行——后处理在严重缺氧后3小时（早期后处理）或24小时（延迟后处理）开始。使用组织学方法和计算机图像分析，在严重缺氧7天后分析海马体和新皮层中神经元的损失情况。严重缺氧导致新皮层第V层中24%的神经元、海马体CA1区中26%的神经元以及CA4区中22%的神经元损失。早期后处理可防止海马体CA1区神经元损失，并显著减少新皮层（降至13%）和CA4区（降至10%）的神经元损失。延迟后处理完全防止了海马体CA4区和新皮层的神经元损伤，并且在很大程度上但并非完全保护了CA1区（12%的神经元损失）。结果表明，低压缺氧进行的后处理具有显著的神经保护作用，减少了脑脆弱结构（海马体和新皮层）中神经元的损失。神经保护的效果取决于首次后处理疗程的呈现时间。
