Gidday J M, Fitzgibbons J C, Shah A R, Park T S
Department of Neurology and Neurological Surgery, St. Louis Children's Hospital, Washington University School of Medicine, MO 63110.
Neurosci Lett. 1994 Feb 28;168(1-2):221-4. doi: 10.1016/0304-3940(94)90455-3.
Very recent studies in adult gerbils and rats have shown that exposure to sublethal ischemia can confer neuroprotection from subsequent lethal ischemic episodes. To determine if a similar phenomenon can be elicited during the perinatal period, we have developed a preconditioning regimen that involves exposure to normothermic hypoxia (8% oxygen) 24 h prior to hypoxia-ischemia in the well-established post-natal-day 7 rat pup model [20]. Significant infarction, manifested as a 34 +/- 4% reduction in cerebral hemispheric weight ipsilateral to the carotid ligation, was noted in control animals (n = 24) one week after hypoxia-ischemia, whereas littermates preconditioned with 3 h hypoxia (n = 29) showed no evidence of hemispheric necrosis. Lack of injury in the latter animals was confirmed at the cellular level by histopathologic analyses of Nissl-stained coronal sections. Thus, pre-exposure to hypoxia induces endogenous adaptive mechanisms that can protect the perinatal brain from hypoxic-ischemic injury.
近期对成年沙鼠和大鼠的研究表明，暴露于亚致死性缺血可使大脑对随后的致死性缺血发作产生神经保护作用。为了确定围生期是否也能引发类似现象，我们制定了一种预处理方案，即在已确立的出生后第7天大鼠幼崽模型中，于缺氧缺血前24小时使其暴露于常温低氧环境（8%氧气）[20]。在缺氧缺血一周后，对照动物（n = 24）出现了明显的梗死，表现为结扎颈动脉同侧大脑半球重量减少34±4%，而经3小时低氧预处理的同窝幼崽（n = 29）未显示出半球坏死的迹象。通过对尼氏染色冠状切片的组织病理学分析，在细胞水平证实了后一组动物未受损伤。因此，预先暴露于低氧环境可诱导内源性适应机制，从而保护围生期大脑免受缺氧缺血性损伤。
