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Hypoxic pretreatment protects against neuronal damage of the rat hippocampus induced by severe hypoxia.

机译:缺氧预处理可防止严重缺氧引起的大鼠海马神经元损伤。

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摘要

The present study investigates whether under conditions of successive hypoxic exposures pretreatment with mild (15% O(2)) or moderate (10% O(2)) hypoxia, protects hippocampal neurones against damage induced by severe (3% O(2)) hypoxia. The ultrastructural findings were also correlated with regional superoxide dismutase (SOD) activity changes. In unpretreated rats severe hypoxia induced ultrastructural changes consistent with the aspects of delayed neuronal death (DND). However, in preexposed animals hippocampal damage was attenuated in an inversely proportional way with the severity of the hypoxic pretreatment. The ultrastructural hypoxic tolerance findings were also closely related to increased regional SOD activity levels. Thus the activation of the endogenous antioxidant defense by hypoxic preconditioning, protects against hippocampal damage induced by severe hypoxia. The eventual contribution of increased endogenous adenosine and/or reduced excitotoxicity to induce hypoxic tolerance is discussed.
机译:本研究调查在轻度(15%O(2))或中度(10%O(2))低氧连续低氧暴露预处理的情况下,保护海马神经元免受严重(3%O(2))诱导的损害缺氧。超微结构的发现还与区域超氧化物歧化酶(SOD)活性变化相关。在未经预处理的大鼠中,严重的缺氧诱导的超微结构改变与延迟神经元死亡(DND)的方面一致。然而,在低氧预处理中,海马损伤的程度与低氧预处理的严重程度成反比。超微结构低氧耐受性的发现也与增加的区域SOD活性水平密切相关。因此,通过低氧预处理激活内源性抗氧化剂防御,可防止严重缺氧引起的海马损伤。讨论了内源性腺苷增加和/或兴奋性毒性降低导致低氧耐受性的最终贡献。

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