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为探讨新生儿缺氧缺血性脑病（ＨＩＥ）的发病机理。将１６只新生猪随机分为正常对照组和ＨＩＥ后２４小时组，以分离的新生猪前脑皮层粗制突触膜（ｓｙｎａｐｔｉｃｍｅｍｂｒａｎｅ，ＳＰＭ）为受体制剂，检测两组动物ＳＰＭ上谷氨酸受体（ＧｌｕＲ），并同时查红细胞胞浆游离钙。结果发现ＨＩＥ后２４小时组的ＧｌｕＲ最大结合位点数为１２．４±２．１ｐｍｏｌ／ｍｇ蛋白，明显低于正常对照组（１７．４±３．１ｐｍｏｌ／ｍｇ蛋白），亲和力（Ｋｄ）差异无统计学意义（Ｐ＞０．０５）；而其红细胞胞浆游离钙〔２．０１±０．１８（Ｆ３３５／Ｆ３８５）〕却明显高于正常组（１．７８±０．２４），且病理学检查损害明显。结论：ＧｌｕＲ及钙离子的变化参与了缺氧缺血性脑损伤的发病
To explore the pathogenesis of neonatal hypoxic-ischemic encephalopathy (HIE). Sixteen newborn pigs were randomly divided into normal control group and 24 h post-HIE group. Synaptic membrane (SPM) Body (GluR), and at the same time check the cytoplasm free calcium. The results showed that the maximum number of GluR binding sites in 24 hours after HIE was 12.4 ± 2.1 pmol / mg protein, which was significantly lower than that of the normal control group (17.4 ± 3.1 pmol / mg protein). The difference in affinity (Kd) (P> 0.05), but the cytoplasmic free calcium [2.01 ± 0.18 (F335 / F385)] was significantly higher than the normal group (1.78 ± 0.24), and the disease Neutropenia obvious damage. Conclusion: The changes of GluR and Ca2 + are involved in the pathogenesis of hypoxic-ischemic brain damage