title: Optically measured NADH concentrations are unaffected by propofol induced EEG silence during transient cerebral hypoperfusion in anesthetized rabbits.
abstract: The neuroprotective benefit of intra-operative anesthetics is widely described and routinely aimed to invoke electroencephalographic (EEG) silence in anticipation of transient cerebral ischemia. Previous rat survival studies have questioned an additional benefit from achieving EEG silence during transient global cerebral hypoperfusion. Surgical preparation on twelve New Zealand white rabbits under ketamine-propofol anesthesia, included placement of skull screws for bilateral EEG monitoring, skull shaving for laser Doppler probes, and a 5 mm diameter right temporal craniotomy for the NADH probe. Transient global cerebral hypoperfusion was achieved with bilateral internal carotid artery occlusion and pharmacologically induced systemic hypotension. All animals acted as controls, and had cerebral hypoperfusion under baseline propofol anesthesia with an active EEG. Thereafter, animals were randomized to receive bolus injection of intracarotid (3-5 mg) or intravenous (10-20 mg) 1% propofol to create EEG silence for 1-2 min. The data collected at baseline, peak hypoperfusion, and 5 and 10 min post hypoperfusion was analyzed by repeated measures ANOVA with post hoc Bonferroni-Dunn test. Eleven of the twelve rabbits completed the protocol. Hemodynamics and cerebral blood flow changes were comparable in all the animals. Compared to controls, the increase in NADH during ischemia was unaffected by EEG silence with either intravenous or intraarterial propofol. We failed to observe any significant additional attenuation of the elevation in NADH levels with propofol induced EEG silence during transient global cerebral hypoperfusion. This is consistent with previous rat survival studies showing that EEG silence was not required for full neuroprotective effects of pentothal anesthesia.
authors.affiliation: Department of Anesthesiology, Columbia University, USA.
authors.forename: Mei
authors.initials: M
authors.lastname: Wang
authors.forename: Sachin
authors.initials: S
authors.lastname: Agarwal
authors.forename: Avraham
authors.initials: A
authors.lastname: Mayevsky
authors.forename: Shailendra
authors.initials: S
authors.lastname: Joshi
mesh_terms: D018686:Anesthetics, Intravenous / Q000494:pharmacology; D000818:Animals; D001921:Brain / Q000098:blood supply / Q000187:drug effects* / Q000201:enzymology; D058256:Brain Waves / Q000187:drug effects / Q000502:physiology; D002560:Cerebrovascular Circulation / Q000187:drug effects / Q000502:physiology; D004195:Disease Models, Animal; D004569:Electroencephalography / Q000187:drug effects*; D002546:Ischemic Attack, Transient / Q000188:drug therapy* / Q000201:enzymology / Q000503:physiopathology*; D009243:NAD / Q000378:metabolism*; D018696:Neuroprotective Agents / Q000494:pharmacology; D015742:Propofol / Q000494:pharmacology*; D011817:Rabbits
chemical_list: D018686:Anesthetics, Intravenous; D018696:Neuroprotective Agents; D009243:NAD; D015742:Propofol