The Fetal Physiology and Neuroscience Group, Department of Physiology, The University of Auckland, Auckland, New Zealand.
J Cereb Blood Flow Metab. 2024 Aug;44(8):1376-1392. doi: 10.1177/0271678X241236014. Epub 2024 Feb 28.
Antenatal hypoxia-ischaemia (HI) in preterm fetal sheep can trigger delayed evolution of severe, cystic white matter injury (WMI), in a similar timecourse to WMI in preterm infants. We therefore examined how severe hypoxia-ischaemia affects recovery of electroencephalographic (EEG) activity. Chronically instrumented preterm fetal sheep (0.7 gestation) received 25 min of complete umbilical cord occlusion (UCO, n = 9) or sham occlusion (controls, n = 9), and recovered for 21 days. HI was associated with a shift to lower frequency EEG activity for the first 5 days with persisting loss of EEG power in the delta and theta bands, and initial loss of power in the alpha and beta bands in the first 14 days of recovery. In the final 3 days of recovery, there was a marked rhythmic shift towards higher frequency EEG activity after UCO. The UCO group spent less time in high-voltage sleep, and in the early evening (7:02 pm ± 47 min) abruptly stopped cycling between sleep states, with a shift to a high frequency state for 2 h 48 min ± 40 min, with tonic electromyographic activity. These findings demonstrate persisting EEG and sleep state dysmaturation after severe hypoxia-ischaemia. Loss of fetal or neonatal sleep state cycling in the early evening may be a useful biomarker for evolving cystic WMI.
产前缺氧缺血（HI）可在早产胎儿羊中引发严重囊性白质损伤（WMI）的延迟演变，其时间进程与早产儿 WMI 相似。因此，我们研究了严重缺氧缺血如何影响脑电图（EEG）活动的恢复。慢性仪器化早产胎儿羊（0.7 孕龄）接受 25 分钟完全脐带结扎（UCO，n=9）或假结扎（对照组，n=9），并恢复 21 天。HI 与前 5 天的 EEG 活动向低频转移相关，随后在恢复的前 14 天中，delta 和 theta 波段的 EEG 功率持续丧失，alpha 和 beta 波段的初始功率丧失。在恢复的最后 3 天，UCO 后出现明显的向高频 EEG 活动的节律性转移。UCO 组在高电压睡眠中的时间减少，并且在傍晚（晚上 7:02 ± 47 分钟）突然停止睡眠状态之间的循环，转变为高频状态持续 2 小时 48 分钟 ± 40 分钟，伴有强直性肌电图活动。这些发现表明严重缺氧缺血后 EEG 和睡眠状态发育不成熟持续存在。傍晚时胎儿或新生儿睡眠状态循环的丧失可能是囊性 WMI 进展的有用生物标志物。
