The Effects of Propofol on Brain Electrical Activity, Neurologic Outcome, and Neuronal Damage Following Incomplete Ischemia in Rats

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Abstract
This study compares the effects of propofol and fentanyl/N2O on spontaneous brain electrical activity, neurologic outcome, and neuronal damage due to incomplete cerebral ischemia in rats. Thirty Sprague-Dawley rats were assigned to one of three groups: group 1 (n = 10) received 70% N2O in O2 plus fentanyl (bolus 10 μg.kg-1, infusion 25 μg.kg-1.h-1); group 2 (n = 10) received 70% N2 in O2 and propofol (infusion 0.8–1.2 mg.kg-1.min-1) adjusted to maintain EEG bunt suppression during ischemia; group 3 (n = 10) was anesthetized with propofol and received 6 ml.kg-110% glucose intraperitoneally 15 min before the start of ischemia. Incomplete cerebral ischemia was produced by right common carotid artery occlusion combined with hemorrhagic hypotension (35 mmHg) for 30 min. Arterial blood gases, pH, and rectal temperature were kept constant in all groups. Plasma glucose was lower during ischemia in propofolanesthetized rats compared to that in fentanyl/N2O- (P = 0.009) and glucose-loaded propofol-treated rats (P = 0.008). Neurologic outcome and brain tissue injury were significantly better in propofol-anesthetized compared to fentanyl/N2O-anesthetized rats (P < 0.05). Elevated plasma glucose in propofol-treated rats resulted in similar neurologic outcome and histopathologic injury as seen in propofolanesthetized rats given no glucose. Recovery of EEG θ–α activity after ischemia was inversely correlated to neurologic deficit (fentanyl/N2O: r = –0.71; propofol: r = –0.83; P < 0.01). These results show that propofol improves neurologic outcome and decreases neuronal damage from incomplete cerebral ischemia when compared to fentanyl/N2O. This effect is not dependent on plasma glucose. Improved neurologic outcome is indicated by early postischemic EEG recovery.

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