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目的：探讨红细胞膜ＡＴＰ酶和氧自由基在新生儿缺氧缺血性脑病（ＨＩＥ）发病中的作用，寻找防治途径。方法：采用孔雀绿分析法检测了３２例新生儿缺氧缺血性脑病时红细胞膜Ｎａ＋Ｋ＋ＡＴＰ酶活性及脂质过氧化代谢产物丙二醛（ＭＤＡ）含量和磷酸肌酸激酶脑型同功酶（ＣＫＢＢ）活性。结果：缺氧缺血性脑病患儿红细胞膜Ｎａ＋Ｋ＋ＡＴＰ酶活性〔（０．１１３±０．０２２）ｎｍｏｌＰｉ·ｈ－１／ｍｇＰｒ〕明显低于正常新生儿〔（０．２９４±０．０３７）ｎｍｏｌＰｉ·ｈ－１／ｍｇＰｒ〕，ＭＤＡ及ＣＫＢＢ活性明显高于正常新生儿，且红细胞膜Ｎａ＋Ｋ＋ＡＴＰ酶活性与ＭＤＡ水平呈明显负相关（ｒ＝－０．３６０，Ｐ＜０．０５），即Ｎａ＋Ｋ＋ＡＴＰ酶活性的降低与脂质过氧化损伤密切相关。结论：氧自由基损伤可能参与了ＨＩＥ的发病和病理过程，进一步损伤细胞膜Ｎａ＋Ｋ＋ＡＴＰ酶功能，使机体生理功能产生不可逆损伤。故对ＨＩＥ治疗中尽早使用抗氧化剂和保护细胞膜Ｎａ＋Ｋ＋ＡＴＰ酶功能的药物十分必要。
Objective: To investigate the role of erythrocyte membrane ATPase and oxygen free radicals in the pathogenesis of neonatal hypoxic-ischemic encephalopathy (HIE) and to find out the prevention and cure ways. Methods: The activity of Na + K + ATPase and the content of malondialdehyde (MDA) in erythrocyte membrane of 32 neonates with hypoxic-ischemic encephalopathy were detected by using malachite green assay. The phosphorylated creatine kinase CKBB) activity. Results: The Na + K + ATPase activity of erythrocyte membrane in children with hypoxic-ischemic encephalopathy 〔(0.113 ± 0.022) nmolPi · h-1 / mgPr〕 was significantly lower than that of the normal neonatal 〔(0.294 ± 0.037) nmolPi · H-1 / mgPr], MDA and CKBB activity were significantly higher than those of normal neonates, and the activity of Na + K + ATPase in erythrocytes was negatively correlated with MDA level (r = -0.360, P <0.05) Decreased activity and lipid peroxidation damage are closely related. Conclusion: Oxygen free radical injury may be involved in the pathogenesis and pathological process of HIE, further impairing the function of Na + K + ATPase in the cell membrane and causing irreversible damage to the physiological function of the body. Therefore, the early use of anti-HIE treatment and protection of cell membrane Na + K ATP activity of the drug is essential.