Dysmaturation of sleep state and electroencephalographic activity after hypoxia-ischaemia in preterm fetal sheep.

Autor:	Lear CA; The Fetal Physiology and Neuroscience Group, Department of Physiology, The University of Auckland, Auckland, New Zealand., Lear BA; The Fetal Physiology and Neuroscience Group, Department of Physiology, The University of Auckland, Auckland, New Zealand., Davidson JO; The Fetal Physiology and Neuroscience Group, Department of Physiology, The University of Auckland, Auckland, New Zealand., King VJ; The Fetal Physiology and Neuroscience Group, Department of Physiology, The University of Auckland, Auckland, New Zealand., Maeda Y; The Fetal Physiology and Neuroscience Group, Department of Physiology, The University of Auckland, Auckland, New Zealand., McDouall A; The Fetal Physiology and Neuroscience Group, Department of Physiology, The University of Auckland, Auckland, New Zealand., Dhillon SK; The Fetal Physiology and Neuroscience Group, Department of Physiology, The University of Auckland, Auckland, New Zealand., Gunn AJ; The Fetal Physiology and Neuroscience Group, Department of Physiology, The University of Auckland, Auckland, New Zealand., Bennet L; The Fetal Physiology and Neuroscience Group, Department of Physiology, The University of Auckland, Auckland, New Zealand.
Jazyk:	angličtina
Zdroj:	Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism [J Cereb Blood Flow Metab] 2024 Aug; Vol. 44 (8), pp. 1376-1392. Date of Electronic Publication: 2024 Feb 28.
DOI:	10.1177/0271678X241236014
Abstrakt:	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. Competing Interests: Declaration of conflicting interestsThe author(s) declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.
Databáze:	MEDLINE
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