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目的 研究新生儿缺氧缺血性脑病 (HIE)患儿的免疫学变化及其机制 ,为免疫学治疗提供理论依据。 方法 以 4 0例正常新生儿及 4 0例 HIE患儿为对象 ,分别检测脐血、生后 1、3、7、12～ 14 d及 2 6～ 2 8d外周血 T淋巴细胞亚群、血清可溶性白细胞介素 2受体、白细胞介素 (IL ) 6、8以及肿瘤坏死因子α、血浆一氧化氮、免疫球蛋白、补体、红细胞 C3b受体花环率、红细胞免疫复合物花环率等免疫指标的变化 ,并于新生儿生后 2 4 h内取静脉血后即刻应用脉冲多普勒超声检测其大脑中动脉的血流动力学参数。 结果 窒息缺氧与 HIE患儿存在 :(1) T淋巴细胞亚群紊乱 ,如生后 1～ 3dHIE与对照组分别为 CD3+ (6 2± 8) %、(6 5± 10 ) % ,CD4 + (39± 7) %、(46± 8) % ,CD8+ (2 3± 6 ) %、(19± 5 ) % ,CD4 + / CD8+比值 1.8± 0 .7、2 .5± 0 .7。至生后 2 6～ 2 8d时上述各指标间差异均无显著性。(2 ) Ig M与 C3降低。(3)细胞因子表达异常。(4)血流动力学参数 RI与 IL- 6呈负相关 (r=- 0 .0 1,P<0 .0 1) ,与 IL- 8及 TNF- α呈正相关 (r=0 .80、0 .72 ,P<0 .0 1)。 结论 免疫功能紊乱参与了 HIE的发病过程 ,细胞因子对脑血流的异常影响可能是免疫因素导致脑损伤的原因之一。
Objective To study the immunological changes and its mechanism in neonates with hypoxic-ischemic encephalopathy (HIE) and provide a theoretical basis for immunological therapy. Methods Totally 40 neonatal and 40 HIE infants were enrolled in this study. Cord blood, peripheral blood T lymphocyte subsets at 1, 3, 7, 12 to 14, and 26 to 28 days after birth were detected. Serum Soluble interleukin 2 receptor, interleukin 6,8, tumor necrosis factor α, plasma nitric oxide, immunoglobulin, complement, rosette of erythrocyte C3b receptor, erythrocyte immune complex rosette and other immune indexes The changes of hemodynamics of middle cerebral artery were detected by pulsed Doppler ultrasonography immediately after venous blood taken within 24 hours after birth. Results Asphyxia and HIE had the following symptoms: (1) The T lymphocyte subsets were disordered. For example, the levels of CD3 + (6 2 ± 8)%, (6 5 ± 10)% and CD4 + (39 ± 7)%, (46 ± 8)%, CD8 + (23 ± 6)%, (19 ± 5)% and CD4 + / CD8 + ratio of 1.8 ± 0.7,2.5 ± 0. There was no significant difference between the above indexes between 26 and 28 days after birth. (2) Ig M and C3 decreased. (3) abnormal cytokine expression. (4) The hemodynamic parameters RI were negatively correlated with IL-6 (r = -0.01, P <0.01), and positively correlated with IL-8 and TNF- 0 .72, P <0 .0 1). Conclusion Immune dysfunction is involved in the pathogenesis of HIE. The abnormal effect of cytokines on cerebral blood flow may be one of the reasons of immune-induced brain injury.