title: The effects of etomidate on cerebral metabolism and blood flow in a canine model for hypoperfusion.
abstract: The effects of etomidate, a nonbarbiturate cerebral metabolic depressant, on cerebral metabolism and blood flow were studied in 29 dogs during cerebral hypoperfusion. Three groups of animals were studied during a 45-minute normotensive and a 30-minute hypotensive period: 10 control animals without etomidate, 11 animals receiving a 0.1-mg/kg etomidate bolus followed by an infusion of 0.05 mg/kg/min etomidate (low-dose group), and eight animals receiving doses of etomidate sufficient to suppress electroencephalographic bursts (high-dose group). The mean arterial pressure fell to similar levels (p less than 0.05) during hypotension in all three groups (40 +/- 5, 38 +/- 3, and 27 +/- 6 mm Hg, respectively). The mean cerebral oxygen extraction fraction rose (p less than 0.05) from 0.23 +/- 0.02 to 0.55 +/- 0.08 in the five control animals tested and from 0.33 +/- 0.02 to 0.53 +/- 0.02 in the seven animals tested in the low-dose group, but did not increase (p greater than 0.05) in the four animals tested in the high-dose group (0.24 +/- 0.03 to 0.23 +/- 0.05). Mean cerebral blood flow levels decreased in all groups during hypotension (p less than 0.05): 42 +/- 3 to 21 +/- 4 ml/100 gm/min (52% +/- 12% decrease) in the five animals tested in the control group, 60 +/- 8 to 24 +/- 6 ml/100 gm/min (56% +/- 13% decrease) in the four animals tested in the low-dose group, and 55 +/- 8 to 22 +/- 3 ml/100 gm/min (60% +/- 4% decrease) in the four animals tested in the high-dose group. In summary, the cerebral oxygen extraction fraction increased in the control animals and low-dose recipients during hypotension, suggesting the presence of threatened cerebral tissue. In contrast, the cerebral oxygen extraction did not change during hypotension when high-dose etomidate was administered. It is concluded that high-dose etomidate may preserve the cerebral metabolic state during hypotension in the present model.
authors.affiliation: Department of Neurological Surgery, University of Texas Southwestern Medical Center, Dallas.
authors.forename: R T
authors.initials: RT
authors.lastname: Frizzell
authors.forename: Y J
authors.initials: YJ
authors.lastname: Meyer
authors.forename: D J
authors.initials: DJ
authors.lastname: Borchers
authors.forename: B E
authors.initials: BE
authors.lastname: Weprin
authors.forename: E C
authors.initials: EC
authors.lastname: Allen
authors.forename: W R
authors.initials: WR
authors.lastname: Pogue
authors.forename: J S
authors.initials: JS
authors.lastname: Reisch
authors.forename: A D
authors.initials: AD
authors.lastname: Cherrington
authors.forename: H H
authors.initials: HH
authors.lastname: Batjer
mesh_terms: D000818:Animals; D001158:Arteries; D001786:Blood Glucose / Q000032:analysis; D001794:Blood Pressure; D001921:Brain / Q000378:metabolism*; D002560:Cerebrovascular Circulation / Q000187:drug effects*; D004285:Dogs; D005045:Etomidate / Q000494:pharmacology*; D005740:Gases / Q000097:blood; D006339:Heart Rate; D007022:Hypotension / Q000139:chemically induced* / Q000378:metabolism / Q000503:physiopathology; D007773:Lactates / Q000097:blood; D019344:Lactic Acid; D010101:Oxygen Consumption
chemical_list: D001786:Blood Glucose; D005740:Gases; D007773:Lactates; D019344:Lactic Acid; D005045:Etomidate