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Dexmedetomidine, a potent alpha 2-agonist, does not affect neuronal damage following severe forebrain ischaemia in
B R Karlsson1, E M Löberg, P A Steen
1Institute for Experimental Medical Research, Ullevål University Hospital, Oslo, Norway.
Abstract:
Central sympathetic activation with increased release of noradrenaline occurs during cerebral ischaemia, but it is not certain how the increased sympathetic activity affects neuronal damage. We have studied the effect of dexmedetomidine, a potent alpha 2-adrenergic receptor agonist that reduces the central release of noradrenaline, on neuronal damage after 10 min of severe forebrain ischaemia in the rat. Ischaemia was achieved by bilateral carotid artery occlusion combined with bleeding to a mean arterial pressure of 50 mmHg. The post-ischaemic neuronal damage was most pronounced in the hippocampal CA1 region (median percentage of necrotic cells 36% (11-69%) and 42% (11-68%) in the dexmedetomidine and vehicle groups, respectively) and in the subiculum. The reticular thalamic nucleus was moderately damaged in all but one rat, while the rest of the thalamus was almost spared. Most rats had mild to moderate damage in cortex and caudoputamen. Dexmedetomidine did not affect the neuronal outcome in this model.