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首页> 外文期刊>Pediatrics: Official Publication of the American Academy of Pediatrics >Neuroprotection with prolonged head cooling started before postischemic seizures in fetal sheep.
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Neuroprotection with prolonged head cooling started before postischemic seizures in fetal sheep.

机译：胎儿绵羊缺血性癫痫发作之前，开始进行长期头部冷却的神经保护。

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OBJECTIVE: Cerebral hypothermia has been shown to reduce damage from experimental hy-poxia-ischemia if started shortly after reperfusion. However, in the newborn infant it may not be feasible to determine prognosis so soon after exposure to asphyxia. The aim of this study was to determine whether head cooling, delayed until shortly before the onset of postasphyxial seizure activity, is neuroprotective. METHODS: Unanesthetized near-term fetal sheep in utero were subjected to 30 minutes of cerebral ischemia. Later, at 5.5 hours, they were randomized to either cooling (n = 7) or sham cooling (n = 10) for 72 hours. Intrauterine cooling was induced by circulating cold water through a coil around the fetal head. The water temperature was titrated to reduce fetal extradural temperature from 39.1 +/- 0.1 degreesC to between 30 degreesC and 33 degreesC, while maintaining esophageal temperature >37 degreesC. RESULTS: Cerebral cooling suppressed the secondary rise in cortical impedance (a measure of cytotoxic edema), but did not prevent delayed seizures, 8 to 30 hours after ischemia. Transient metabolic changes including increased plasma lactate and glucose levels were seen with a moderate sustained rise in blood pressure. This severe cerebral insult resulted in depressed residual parietal electroencephalographic activity after 5 days recovery (-14.2 +/- 1.5 decibels), associated with a watershed distribution of neuronal loss (eg, 94 +/- 4% in parasagittal cortex and 77 +/- 4% in the lateral cortex). Hypothermia was associated with better recovery of electroencephalographic activity (-8.9% +/- 1.8 decibels) and substantially reduced neuronal loss in the parasagittal cortex (46 +/- 13%), the lateral cortex (9 +/- 4%), and other regions except the cornu ammonis sectors 1 and 2 of the hippocampus. CONCLUSIONS: Delayed selective head cooling begun before the onset of postischemic seizures and continued for 3 days may have potential to significantly improve the outcome of moderate to severe hypoxic-ischemic encephalopathy.
机译：目的：显示脑低温可减少再灌注后立即开始的实验性缺氧缺血性损伤。然而，在新生儿中，窒息后不久就可能无法确定预后。这项研究的目的是确定延迟到窒息后癫痫发作开始之前不久的头部冷却是否具有神经保护作用。方法：未麻醉的胎儿在子宫内进行30分钟的脑缺血。之后，在5.5小时，将它们随机分配到冷却（n = 7）或假冷却（n = 10）72小时。通过使冷水通过绕胎儿头的线圈循环来引起宫内冷却。滴定水温以将胎儿硬膜外温度从39.1 +/- 0.1摄氏度降低到30摄氏度和33摄氏度之间，同时保持食管温度> 37摄氏度。结果：脑冷却抑制了皮层阻抗的继发性升高（一种衡量细胞毒性水肿的指标），但并没有阻止缺血后8至30小时的癫痫发作的延迟。观察到短暂的代谢变化，包括血浆乳酸和葡萄糖水平升高，血压持续中度升高。这种严重的脑损伤导致恢复5天后残余顶壁脑电图活动降低（-14.2 +/- 1.5分贝），与神经元丢失的分水岭分布有关（例如，矢状旁神经皮层为94 +/- 4％，神经元为77 +/-在外侧皮质中占4％）。体温过低可以使脑电图活动恢复更好（-8.9％+/- 1.8分贝），并显着减少矢状旁旁皮质（46 +/- 13％），外侧皮质（9 +/- 4％）和除海马角膜第1和第2扇区外的其他区域。结论：选择性的头部降温延迟发作始于缺血性发作之前，持续3天可能会显着改善中度至重度缺氧缺血性脑病的预后。

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