Cerebral hypothermia is not neuroprotective when started after postischemic seizures in fetal sheep
Cerebral hypothermia is not neuroprotective when started after postischemic seizures in fetal sheep
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DOI：
10.1203/00006450-199909000-00005
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发表时间：
1999-09-01
影响因子：
3.6
通讯作者：
Gunn, TR
中科院分区：
文献类型：
--
作者：
Gunn, AJ;Bennet, L;Gunn, TR
如果在缺氧缺血后数小时内开始，长时间的脑低温具有神经保护作用，然而，延迟性癫痫活动是围产期窒息后不良预后的主要临床指标之一。本研究的目的是确定延迟至窒息后癫痫发作后的头部冷却是否仍具有神经保护作用。未麻醉的近足月胎羊在子宫内接受双侧颈动脉闭塞引起的30分钟的脑缺血。八个半小时后，他们接受冷却 (n = 5) 或假冷却 (n = 13)，直到侮辱后 72 小时。通过通过胎儿头部周围的线圈循环冷水诱导宫内冷却，滴定将胎儿硬膜外温度从 39.4 +/- 0.1 摄氏度降低到 30 至 33 摄氏度之间。脑缺血导致强烈癫痫样活动延迟发展，从撞击后 6 至 8 小时，随后皮质阻抗（细胞毒性水肿的测量）和颈动脉血流显着继发性升高。大脑冷却显着减弱了阻抗的继发性上升和颈动脉血流量的减少（p < 0.001）。恢复 5 天后，与对照组相比，低温下顶叶 EEG 活动相对于基线的丧失（-12.5 +/- 1.4 与 -15.2 +/- 1.2 dB，平均值 +/-：SEM，NS）或矢状旁皮质神经元丧失（82 +/- 9 与 90 +/- 5%，NS）没有显着差异。总之，缺血后癫痫发作后开始的延迟长时间头部冷却并不能起到神经保护作用。这些数据强调了在再灌注后、继发性损伤发生之前的潜伏期进行干预的重要性。
Prolonged cerebral hypothermia is neuroprotective if started within a few hours of hypoxia-ischemia, However, delayed seizure activity is one of the major clinical indicators of an adverse prognosis after perinatal asphyxia. The aim of this study was to determine whether head cooling delayed until after the onset of postasphyxial seizures may still be neuroprotective. Unanesthetized near-term fetal sheep in utero received 30 min of cerebral ischemia induced by bilateral carotid artery occlusion. Eight and one-half hours later, they received either cooling (n = 5) or sham cooling (n = 13) until 72 h after the insult. Intrauterine cooling, induced by circulating cold water through a coil around the fetal head, was titrated to reduce fetal extradural temperature from 39.4 +/- 0.1 degrees C to between 30 and 33 degrees C, Cerebral ischemia led to the delayed development of intense epileptiform activity from 6 to 8 h postinsult, followed by a marked secondary rise in cortical impedance (a measure of cytotoxic edema) and in carotid blood flow. Cerebral cooling markedly attenuated the secondary rise in impedance and reduced carotid blood flow (p < 0.001). After 5 d recovery, there was no significant difference in loss of parietal EEG activity relative to baseline in the hypothermia compared with the control group (-12,5 +/- 1.4 ver sus -15.2 +/- 1.2 dB, mean +/-: SEM, NS) or in parasagittal cortical neuronal loss (82 +/- 9 versus 90 +/- 5%, NS). In conclusion, delayed prolonged head cooling begun after the onset of postischemic seizures was not neuroprotective. These data highlight the importance of intervention in the latent phase, after reperfusion but before the onset of secondary injury.