Erythropoietin in the cerebrospinal fluid of neonates who sustained CNS injury
Erythropoietin in the cerebrospinal fluid of neonates who sustained CNS injury
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DOI：
10.1203/00006450-199911000-00009
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发表时间：
1999-11-01
影响因子：
3.6
通讯作者：
Christensen, RD
中科院分区：
文献类型：
--
作者：
Juul, SE;Stallings, SA;Christensen, RD
我们以前报道过红细胞生成素（Epo）存在于人脑脊液（CSF）中。目前尚不清楚脑脊液Epo浓度是否在中枢神经系统损伤的情况下发生变化，或者如果发生变化，这种变化是否反映了血脑屏障完整性的丧失或中枢神经系统Epo合成的增加。我们假设脑脊液Epo在包括缺氧、脑膜炎和脑室内出血（IVH）在内的神经损伤情况下增加，并且脑脊液Epo浓度与血浆Epo浓度无关。为了验证这些假设，我们测量了122对新生儿和儿童的脑脊液和血液样本中的Epo浓度，分类如下：16，窒息；31、脑膜炎;Il IVH;41岁的控制。12名接受重组促红细胞生成素（rEpo）治疗的婴儿和另外11名患有各种神经问题的儿童样本也进行了评估。窒息婴儿脑脊液和血浆Epo浓度显著高于对照组（225.0 +/- 155.0 vs 4.5 +/- 0.5 mU/mL；脑脊液平均+/- SEM， p < 0.05；血浆1806.7 +/- 1254 vs 5.2 +/- 0.5, p < 0.05）。IVH患儿脑脊液Epo浓度高于对照组（p < 0.01），血浆Epo浓度不高于对照组。脑膜炎患者没有脑脊液或血浆促红细胞生成素浓度升高。在接受rEpo治疗的婴儿中，脑脊液和血浆Epo浓度没有相关性。我们得出结论，Epo在脑脊液中因缺氧而选择性增加，IVH则较少，而脑膜炎则完全没有。rEpo治疗不提高脑脊液Epo。这些发现表明，促红细胞生成素不会穿过血脑屏障，缺氧诱导中枢神经系统促红细胞生成素合成增加。
We previously reported that erythropoietin (Epo) is present in human cerebrospinal fluid (CSF). It is not known whether CSF Epo concentrations change under conditions of CNS injury or, if so, whether this change reflects loss of blood-brain barrier integrity or increased CNS Epo synthesis. We hypothesized that CSF Epo increases in conditions of neural injury including hypoxia, meningitis, and intraventricular hemorrhage (IVH) and that CSF Epo concentrations are independent of plasma Epo concentrations. To test these hypotheses, Epo concentrations were measured in 122 paired CSF and blood samples obtained from neonates and children categorized as follows: 16, asphyxia; 31, meningitis; Il, IVH; 41, controls. Twelve infants treated with recombinant Epo (rEpo) and 11 additional samples from children with miscellaneous neurologic problems were also evaluated. CSF and plasma Epo concentrations were significantly higher in asphyxiated infants than in controls (225.0 +/- 155.0 versus 4.5 +/- 0.5 mU/mL; mean +/- SEM, p < 0.05, respectively, in CSF; 1806.7 +/- 1254 versus 5.2 +/- 0.5, p < 0.05 in plasma). Neonates with IVH had higher CSF Epo concentrations than controls (p < 0.01) but did not have higher plasma Epo concentrations than controls. Patients with meningitis did not have elevated CSF or plasma Epo concentrations. There was no correlation between CSF and plasma Epo concentrations in infants treated with rEpo. We conclude that Epo is selectively increased in the CSF by hypoxia, less so by IVH, and not at all by meningitis. rEpo treatment does not elevate CSF Epo. These findings suggest that rEpo does not cross the blood-brain barrier and that hypoxia induces increased CNS synthesis of Epo.