Protection of axonal integrity with 48 or 72 h of cerebral hypothermia in near-term fetal sheep.

作者: Kelly Q. Zhou , Vittoria Draghi , Christopher A. Lear , Justin M. Dean , Jesse L. Ashton

DOI: 10.1038/S41390-019-0475-8

关键词: Myelin basic proteinEncephalopathyMicrogliaPathologyIschemiaMyelinMedicineHypothermiaFetusWhite matter

摘要: Therapeutic hypothermia is partially protective for neonatal hypoxic–ischemic encephalopathy (HIE). Damage to the white matter tracts highly associated with adverse outcomes after HIE, but effectiveness and optimal duration of attenuate axonal injury are unclear. Near-term fetal sheep were randomized sham control or cerebral ischemia 30 min normothermia from 3 either 48 72 h. Sheep killed 7 days. SMI-312-labeled axons myelin basic protein quantified in intragyral first second parasagittal gyri. Ischemia was reduced area fraction (p < 0.05); loss linearity thin, sparse axons, spheroids, compared dense, linear morphology controls induction microglia an amoeboid morphology. Both ischemia–48 h ischemia–72 h improved (p < 0.05), although abnormal morphological features seen a subset. Microglial suppressed by hypothermia, ramified These data suggest that therapeutic can alleviate post-ischemic axonopathy, part suppressing secondary inflammation.

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