The effects of etomidate on cerebral metabolism and blood flow in a canine model for hypoperfusion

R. Tyler Frizzell, Y. J. Meyer, D. J. Borchers, B. E. Weprin, E. C. Allen, W. R. Pogue, J. S. Reisch, A. D. Cherrington, H. Hunt Batjer

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Abstract

The effects of etomidate, a nonbarbiturate cerebral metabolic depressant, on cerebra1 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 anima1s 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 arteria1 pressure fell to similar levels (p < 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 < 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 > 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 < 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 ose etomidate may preserve the cerebral metabolic state during hypotension in the present model.

Original languageEnglish (US)
Pages (from-to)263-269
Number of pages7
JournalJournal of Neurosurgery
Volume74
Issue number2
StatePublished - 1991

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Cerebrovascular Circulation
Etomidate
Canidae
Hypotension
Oxygen
Dogs

Keywords

  • cerebral blood flow
  • cerebral metabolism
  • etomidate

ASJC Scopus subject areas

  • Clinical Neurology
  • Neuroscience(all)

Cite this

Tyler Frizzell, R., Meyer, Y. J., Borchers, D. J., Weprin, B. E., Allen, E. C., Pogue, W. R., ... Hunt Batjer, H. (1991). The effects of etomidate on cerebral metabolism and blood flow in a canine model for hypoperfusion. Journal of Neurosurgery, 74(2), 263-269.

The effects of etomidate on cerebral metabolism and blood flow in a canine model for hypoperfusion. / Tyler Frizzell, R.; Meyer, Y. J.; Borchers, D. J.; Weprin, B. E.; Allen, E. C.; Pogue, W. R.; Reisch, J. S.; Cherrington, A. D.; Hunt Batjer, H.

In: Journal of Neurosurgery, Vol. 74, No. 2, 1991, p. 263-269.

Research output: Contribution to journalArticle

Tyler Frizzell, R, Meyer, YJ, Borchers, DJ, Weprin, BE, Allen, EC, Pogue, WR, Reisch, JS, Cherrington, AD & Hunt Batjer, H 1991, 'The effects of etomidate on cerebral metabolism and blood flow in a canine model for hypoperfusion', Journal of Neurosurgery, vol. 74, no. 2, pp. 263-269.
Tyler Frizzell R, Meyer YJ, Borchers DJ, Weprin BE, Allen EC, Pogue WR et al. The effects of etomidate on cerebral metabolism and blood flow in a canine model for hypoperfusion. Journal of Neurosurgery. 1991;74(2):263-269.
Tyler Frizzell, R. ; Meyer, Y. J. ; Borchers, D. J. ; Weprin, B. E. ; Allen, E. C. ; Pogue, W. R. ; Reisch, J. S. ; Cherrington, A. D. ; Hunt Batjer, H. / The effects of etomidate on cerebral metabolism and blood flow in a canine model for hypoperfusion. In: Journal of Neurosurgery. 1991 ; Vol. 74, No. 2. pp. 263-269.
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abstract = "The effects of etomidate, a nonbarbiturate cerebral metabolic depressant, on cerebra1 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 anima1s 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 arteria1 pressure fell to similar levels (p < 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 < 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 > 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 < 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 ose etomidate may preserve the cerebral metabolic state during hypotension in the present model.",
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AU - Meyer, Y. J.

AU - Borchers, D. J.

AU - Weprin, B. E.

AU - Allen, E. C.

AU - Pogue, W. R.

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AU - Cherrington, A. D.

AU - Hunt Batjer, H.

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N2 - The effects of etomidate, a nonbarbiturate cerebral metabolic depressant, on cerebra1 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 anima1s 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 arteria1 pressure fell to similar levels (p < 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 < 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 > 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 < 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 ose etomidate may preserve the cerebral metabolic state during hypotension in the present model.

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