title: The effects of propofol on brain electrical activity, neurologic outcome, and neuronal damage following incomplete ischemia in rats.
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 micrograms.kg-1, infusion 25 micrograms.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 burst suppression during ischemia; group 3 (n = 10) was anesthetized with propofol and received 6 ml.kg-1 10% 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 propofol-anesthetized 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 less than 0.05). Elevated plasma glucose in propofol-treated rats resulted in similar neurologic outcome and histopathologic injury as seen in propofol-anesthetized rats given no glucose. Recovery of EEG theta-alpha activity after ischemia was inversely correlated to neurologic deficit (fentanyl/N2O: r = -0.71; propofol: r = -0.83; P less than 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.(ABSTRACT TRUNCATED AT 250 WORDS)
authors.affiliation: Department of Anesthesiology, University Hospital Eppendorf, Hamburg, Germany.
authors.forename: E
authors.initials: E
authors.lastname: Kochs
authors.forename: W E
authors.initials: WE
authors.lastname: Hoffman
authors.forename: C
authors.initials: C
authors.lastname: Werner
authors.forename: C
authors.initials: C
authors.lastname: Thomas
authors.forename: R F
authors.initials: RF
authors.lastname: Albrecht
authors.forename: J
authors.initials: J
authors.lastname: Schulte am Esch
mesh_terms: D000818:Animals; D001921:Brain / Q000187:drug effects / Q000503:physiopathology*; D001925:Brain Damage, Chronic / Q000517:prevention & control*; D001927:Brain Diseases / Q000209:etiology* / Q000517:prevention & control; D002545:Brain Ischemia / Q000150:complications* / Q000503:physiopathology; D003864:Depression, Chemical; D004569:Electroencephalography / Q000187:drug effects; D005283:Fentanyl / Q000494:pharmacology; D008297:Male; D015742:Propofol / Q000494:pharmacology*; D051381:Rats; D011919:Rats, Inbred Strains
chemical_list: D005283:Fentanyl; D015742:Propofol