亚低温对新生大鼠缺氧缺血性脑损伤大脑皮质神经元一氧化氮合酶表达及血糖水平的影响

通过亚低温对新生鼠缺氧缺血性脑损伤（ＨＩＢＤ）大脑皮质神经元一氧化氮合酶（ＮＯＳ）及血糖水平影响的研究，探讨亚低温对缺氧缺血性脑损伤的保护作用机制。建立新生鼠缺氧缺血性脑病（ＨＩＥ）标准化动物模型，将其随机分为对照组、３１℃亚低温和３４℃亚低温干预组并设立假手术组，应用免疫组化染色观察大脑皮质区ＮＯＳ阳性神经元数目，并利用微量血糖监测仪测定血糖。结果表明，缺血缺氧后１２ｈ、２４ｈ，亚低温干预组大脑皮质ＮＯＳ阳性神经元数均显著低于对照组，血糖水平均显著高于对照组。３１℃和３４℃亚低温干预两组间各个时期大脑皮质区ＮＯＳ阳性神经元数目及血糖水平无显著差异。亚低温可通过抑制神经元内ＮＯＳ活性，减少过量ＮＯ的生成，以及提高血糖水平，对缺氧缺血性脑损伤鼠大脑神经细胞起到保护作用

EFFECT OF MILD HYPOTHERMIA ON ACTIVITY NITRIC OXIDE SYNTHASE IN CORTICAL NEURONS AND GLYCEMIA LEVELS OF NEONATAL RATS WITH HYPOXIC ISCHEMIC BRAIN DAMAGE

Through investigating the effect of mild hypothermia on activity of nitric oxide synthase(NOS) in cortical neurons and glycemia levels of neonatal rats with hypoxic ischemic brain damage(HIBD).We studied the mechanism of protecting hypoxic ischemic neurons of mild hypothermia.We established neonatal rat HIBD models,used NOS immunohistochemistry and glycemia determination by micromethod.The number of cortical NOS positive neurons after hypoxic ischemia was significantly decreased as compared with controls.The glycemia levels was significantly increased than that controls.No significant difference was found in number of cortical NOS positive neurons and glycemia levels between 31℃ and 34℃ mild hypothemia. The results imply that hypothermia can decrease overproduction of NO through inhibiting the increase of the activity of NOS,and increase the glycemia levels,thus protect the hypoxic ischemic neurons.