作者: Justin M. Dean , Sherly George , Andrew S. Naylor , Carina Mallard , Alistair J. Gunn
DOI: 10.1016/J.NEUROPHARM.2008.05.009
关键词: Agonist 、 Gestation 、 Blockade 、 Neuroprotection 、 Adrenergic receptor 、 Endocrinology 、 Umbilical Cord Occlusion 、 Clonidine 、 Medicine 、 Fetus 、 Internal medicine
摘要: Abstract We have previously shown that brief α 2 -adrenergic receptor blockade increased neuronal injury after severe hypoxia in preterm fetal sheep. now examine whether infusion of an agonist, clonidine, is neuroprotective. Preterm sheep (70% gestation) received either saline-vehicle or clonidine at 10 μg/kg/h (low-dose) 100 μg/kg/h (high-dose) from 15 min until 4 h 25 min umbilical cord occlusion. Both low- and high-dose infusions sham-occlusion were associated with transient EEG suppression but no loss. Low-dose not occlusion a significant overall increase numbers surviving neurons three days' recovery. High-dose was hyperglycemia delayed electrographic seizures. These results provide further evidence activation shortly perinatal hypoxia–ischemia can promote neural recovery, highlight the complex dose–response exogenous therapy.