| Background: Dopamine is an attractive and important neurotransmitter in neurobiological study. It involves multiple functions ranging from movement, cognition, respiration and reinforcement to neurological disorders. Extensive data indicate that dopamine plays an important role in hypoxia-ischemia cerebral injury. Objective: The present study evaluated the effects of propofol on dopamine release in a rat hippocampus model of hypoxia-ischemia injury by using carbon fiber microelectrode (CFE) electrochemical technique in vivo. Methods: First, we utilized CFE electrochemistry technique to quantified the catecholamine release of rat hippocampus CA1 in vivo; second, we set up the model of cerebral hypoxia-ischemic injury; at the end set up the HICS(Hypoxia-ischaemia induced catecholamine signal) model based on the model of HI. Followed by effects of propofol and/or nomifensine on HICS model. Result: HICS could be induced by hypoxia-ischemic cerebral injury in vivo and it could be repeated after 20-30 min. Propofol (1mg iv) pretreatment before hypoxia could significantly inhibit HICS amplitude (34±19.86 vs 22.19±13.13,n=10) (p=0.014) and velocity (0.45±0.27 vs 0.33±0.23, n=10) (p=0.045). Nomifensine (1mg iv)pretreatment before hypoxia could significantly increase HICS amplitude (36.39±21.19 vs 52.96±32.74, n=8) (p=0.023) and accelerate velocity (0.48±0.28 vs 0.78±0.47, n=8) (p=0.010). However,propofol could not reverse the effects of nomifensine on HICS. Conclusion:HICS is an new, stable and reliable signal to estimate neuroprotective effectsin vivo. Our study confirm that propofol can depress HICS significantly,which may suggest that propofol protect cerebral hypoxia-ischemia injury inrat.
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