Journal
JOURNAL OF NEUROIMMUNE PHARMACOLOGY
Volume 11, Issue 2, Pages 238-247Publisher
SPRINGER
DOI: 10.1007/s11481-016-9658-9
Keywords
alpha 2 adrenergic receptors; Dexmedetomidine; Neonates; Neuroprotection; Postconditioning; Rats
Categories
Funding
- National Institutes of Health, Bethesda, MD [R01 GM098308]
- International Anesthesia Research Society, Cleveland, OH
- American Heart Association Mid-Atlantic Affiliate, Baltimore, MD [10GRNT3900019]
- Robert M. Epstein Professorship endowment, University of Virginia, Charlottesville, VA
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Perinatal asphyxia can lead to death and severe disability. Brain hypoxia-ischemia (HI) injury is the major pathophysiology contributing to death and severe disability after perinatal asphyxia. Here, seven-day old Sprague-Dawley rats were subjected to left brain HI. Dexmedetomidine was given intraperitoneally after the brain HI. Yohimbine or atipamezole, two alpha 2 adrenergic receptor antagonists, were given 10 min before the dexmedetomidine injection. Neurological outcome was evaluated 7 or 28 days after the brain HI. Frontal cerebral cortex was harvested 6 h after the brain HI. Left brain HI reduced the left cerebral hemisphere weight assessed 7 days after the brain HI. This brain tissue loss was dose-dependently attenuated by dexmedetomidine. Dexmedetomidine applied within 1 h after the brain HI produced this effect. Dexmedetomidine attenuated the brain HI-induced brain tissue and cell loss as well as neurological and cognitive dysfunction assessed from 28 days after the brain HI. Dexmedetomidine postconditioning-induced neuroprotection was abolished by yohimbine or atipamezole. Brain HI increased tumor necrosis factor alpha and interleukin 1 beta in the brain tissues. This increase was attenuated by dexmedetomidine. Atipamezole inhibited this dexmedetomidine effect. Our results suggest that dexmedetomidine postconditioning reduces HI-induced brain injury in the neonatal rats. This effect may be mediated by alpha 2 adrenergic receptor activation that inhibits inflammation in the ischemic brain tissues.
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