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首页> 外文期刊>Pediatrics: Official Publication of the American Academy of Pediatrics >Vascular endothelial growth factor in the cerebrospinal fluid of infants who died of sudden infant death syndrome: evidence for antecedent hypoxia.
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Vascular endothelial growth factor in the cerebrospinal fluid of infants who died of sudden infant death syndrome: evidence for antecedent hypoxia.

机译：因婴儿猝死综合症而死亡的婴儿的脑脊液中的血管内皮生长因子：先前缺氧的证据。

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OBJECTIVES: Recurrent hypoxemia has been proposed as an important pathophysiological mechanism underlying sudden infant death syndrome (SIDS). However, conflicting results emerged when xanthines were used as markers for hypoxia. The vascular endothelial growth factor (VEGF) gene is highly sensitive to changes in tissue partial oxygen tension, and changes in genomic and protein expression occur even after changes in oxygenation within the physiologic range. METHODS: For determining whether hypoxia precedes SIDS, VEGF levels were measured using an enzyme-linked immunosorbent assay in the cerebrospinal fluid (CSF) of 51 SIDS infants and in 33 additional control infants who died of an identifiable cause. In addition, 6 rats that had a chronically implanted catheter in the lateral ventricle were exposed to a short hypoxic challenge, and VEGF concentrations were measured in CSF at various time points for 24 hours. Another set of 6 rats were killed with a pentobarbital overdose, and VEGF CSF levels were obtained at different time points after death. RESULTS: Mean VEGF concentrations in CSF were 308.2 +/- 299.1 pg/dL in the SIDS group and 85.1 +/- 82.9 pg/dL in those who died of known causes. Mean postmortem delay averaged 22 hours for both groups. In rat experiments, hypoxic exposures induced time-dependent increases in VEGF, peaking at 12 hours and returning to baseline at 24 hours. Postmortem duration in the animals was associated with gradual increases in VEGF that reached significance only at 36 hours. CONCLUSIONS: We conclude that VEGF CSF concentrations are significantly higher in infants who die of SIDS. We postulate that hypoxia is a frequent event that precedes the sudden and unexpected death of these infants.
机译：目的：反复低氧血症被认为是婴儿猝死综合症（SIDS）的重要病理生理机制。然而，当将黄嘌呤用作缺氧的标志物时，出现了矛盾的结果。血管内皮生长因子（VEGF）基因对组织部分氧张力的变化高度敏感，即使在生理范围内的氧合变化后，基因组和蛋白质表达也会发生变化。方法：为了确定缺氧是否先于SIDS，在51名SIDS婴儿的脑脊液（CSF）中和在33名因可查明原因死亡的对照婴儿中，采用酶联免疫吸附法测定了VEGF水平。另外，将6只在侧脑室中长期植入了导管的大鼠暴露于短暂的低氧攻击下，并在24小时的各个时间点测量了CSF中的VEGF浓度。用过量的戊巴比妥杀死另一组6只大鼠，并在死亡后的不同时间点获得VEGF CSF水平。结果：SIDS组中CSF的平均VEGF浓度为308.2 +/- 299.1 pg / dL，死于已知原因的人的平均VEGF浓度为85.1 +/- 82.9 pg / dL。两组的平均验尸延迟平均为22小时。在大鼠实验中，低氧暴露引起VEGF的时间依赖性增加，在12小时达到峰值，并在24小时恢复至基线。动物的死后持续时间与仅在36小时时达到显着水平的VEGF逐渐增加有关。结论：我们得出结论，死于SIDS的婴儿的VEGF CSF浓度明显更高。我们假设低氧是这些婴儿突然和意外死亡之前的常见事件。

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