β2 adrenergic-mediated reduction of blood glutamate levels and improved neurological outcome after traumatic brain injury in rats.

Background: Isoflurane-anesthetized rats subjected to traumatic brain injury (TBI) show a transient reduction in blood L-glutamate levels. Having previously observed that isoproterenol produces a sustained decrease in blood glutamate levels in naive rats, we investigated the possible effects of nonselective and selective β1 and β2 adrenergic agonists and antagonists both on blood glutamate levels and on the neurological outcomes of rats subjected to TBI.

Methods: Rats received either 10 mL/kg of isotonic saline 1 hour after TBI, 50 µg/kg of isoproterenol pretreatment 30 minutes before TBI, 10 mg/kg of propranolol pretreatment 60 minutes before TBI, 10 mg/kg of metoprolol pretreatment 60 minutes before TBI, or 10 mg/kg of butaxamine pretreatment 40 minutes before TBI and 10 minutes before pretreatment with 50 µg/kg isoproterenol or 10 mg/kg of propranolol 60 minutes after TBI.

An experimental model of focal ischemia using an internal carotid artery approach.

Animal models of cerebral ischemia represent an important contribution to both our understanding of stroke mechanism and the development of new therapies. The technique of MCAO (middle cerebral artery occlusion) via ECA (external carotid artery) occlusion is widely utilized. Disruption of the ECA and its branches leads to impaired mastication and oral intake, post-surgical body weight loss, and poor neurological recovery which can possibly confound one's interpretation of rats' neurological outcome.

Regulation of blood L-glutamate levels by stress as a possible brain defense mechanism.

Isoflurane-anesthetized rats submitted to a closed head injury (CHI) display a significant decrease of their blood glutamate levels. Having demonstrated that a decrease of blood L-glutamate (glutamate) causes an increase of the driving force for a spontaneous brain-to-blood glutamate efflux, and consequently affords brain neuroprotection, we investigated here the possible mechanisms which can affect blood glutamate levels. Reasoning that the spontaneous decrease of blood glutamate levels post CHI could be part of a stress response, we observed that the stress involved in tail artery catheterization under isoflurane anesthesia does not affect blood glutamate levels.