کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
2494726 | 1115577 | 2008 | 9 صفحه PDF | دانلود رایگان |
![عکس صفحه اول مقاله: Partial neuroprotection with low-dose infusion of the α2-adrenergic receptor agonist clonidine after severe hypoxia in preterm fetal sheep Partial neuroprotection with low-dose infusion of the α2-adrenergic receptor agonist clonidine after severe hypoxia in preterm fetal sheep](/preview/png/2494726.png)
We have previously shown that brief α2-adrenergic receptor blockade increased neuronal injury after severe hypoxia in preterm fetal sheep. We now examine whether infusion of an α2-adrenergic receptor agonist, clonidine, is neuroprotective. Preterm fetal sheep (70% gestation) received either saline-vehicle or clonidine at either 10 μg/kg/h (low-dose) or 100 μg/kg/h (high-dose) from 15 min until 4 h after 25 min of umbilical cord occlusion. Both low- and high-dose clonidine infusions after sham-occlusion were associated with transient EEG suppression but no neuronal loss. Low-dose but not high-dose clonidine infusions after umbilical cord occlusion were associated with a significant overall increase in numbers of surviving neurons after three days' recovery. High-dose clonidine was associated with transient hyperglycemia and increased numbers of delayed electrographic seizures. These results provide further evidence that α2-adrenergic receptor activation shortly after perinatal hypoxia–ischemia can promote neural recovery, but highlight the complex dose–response of exogenous therapy.
Journal: Neuropharmacology - Volume 55, Issue 2, August 2008, Pages 166–174