Effects of etomidate and hypothermia on cerebral metabolism and blood flow in a canine model of hypoperfusion

R. T. Frizzell, F. M. Fichtel, M. B. Jordan, B. E. Weprin, D. J. Borchers, E. C. Allen, W. R. Pogue, H. H. Batjer

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Abstract

Etomidate is a nonbarbiturate hypnotic agent which, like the barbiturates, decreases the cerebral metabolic rate of oxygen consumption (CMRO2) 35-50%. The present studies assessed whether etomidate decreased CMRO2 through temperature-dependent mechanisms and whether the combination of etomidate and moderate hypothermia (28°C) decreased CMRO2 more than hypothermia alone. Nineteen anesthetized dogs were treated with saline, etomidate (burst- suppressive doses), etomidate with hypothermia, or hypothermia alone. Etomidate did not affect (p > 0.05) the mean arterial pressure (MAP, mm Hg) but modestly lowered the heart rate [HR; 124 ± 6 to 105 ± 14, (mean ± SEM); p < 0.05] whereas hypothermia (without or with etomidate) lowered (p < 0.05) both MAP (141 ± 4 to 116 ± 5 and 135 ± 6 to 81 ± 7) and HR (135 ± 14 to 84 ± 3 and 135 ± 10 to 69 ± 5, respectively). Etomidate administration did not result in a change (p > 0.05) in the esophageal, brain parenchymal, or subdural temperature. CMRO2 (ml/100 g/min) decreased (p < 0.05) during etomidate administration (3.2 ± 0.4 to 1.7 ± 0.2) and hypothermia (3.5 ± 0.2 to 1.1 ± 0.2), but the addition of etomidate to hypothermia did not further reduce CMRO2 in the animals (3.1 ± 0.5 to 1.3 ± 0.2) despite decreasing their brain hemispheric electrical activity from 9 ± 1 Hz to a burst-suppressive state. During hypotension (MAP 30 ± 2) induced by sodium nitroprusside and trimethaphan administration, the cerebral arteriovenous difference in O2 (AVDO2) increased (p < 0.05) in the saline group (5.4 ± 0.9 to 10.7 ± 1.0 ml/dl) but not in the other groups. Thus, etomidate does not have adverse cardiovascular effects associated with moderate hypothermia, and decreases CMRO2 independently of brain temperature changes. Etomidate, however, in this model does not further reduce CMRO2 in moderately hypothermic animals despite decreasing their brain hemispheric electrical activity. Etomidate, hypothermia, and the combination of etomidate and hypothermia all blunt the hypotension-induced increase in cerebral AVDO2.

Original languageEnglish (US)
Pages (from-to)104-110
Number of pages7
JournalJournal of Neurosurgical Anesthesiology
Volume5
Issue number2
StatePublished - 1993

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Cerebrovascular Circulation
Etomidate
Hypothermia
Canidae
Brain
Temperature
Trimethaphan
Controlled Hypotension
Barbiturates
Nitroprusside
Hypnotics and Sedatives

ASJC Scopus subject areas

  • Anesthesiology and Pain Medicine
  • Clinical Neurology

Cite this

Effects of etomidate and hypothermia on cerebral metabolism and blood flow in a canine model of hypoperfusion. / Frizzell, R. T.; Fichtel, F. M.; Jordan, M. B.; Weprin, B. E.; Borchers, D. J.; Allen, E. C.; Pogue, W. R.; Batjer, H. H.

In: Journal of Neurosurgical Anesthesiology, Vol. 5, No. 2, 1993, p. 104-110.

Research output: Contribution to journalArticle

Frizzell, R. T. ; Fichtel, F. M. ; Jordan, M. B. ; Weprin, B. E. ; Borchers, D. J. ; Allen, E. C. ; Pogue, W. R. ; Batjer, H. H. / Effects of etomidate and hypothermia on cerebral metabolism and blood flow in a canine model of hypoperfusion. In: Journal of Neurosurgical Anesthesiology. 1993 ; Vol. 5, No. 2. pp. 104-110.
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abstract = "Etomidate is a nonbarbiturate hypnotic agent which, like the barbiturates, decreases the cerebral metabolic rate of oxygen consumption (CMRO2) 35-50{\%}. The present studies assessed whether etomidate decreased CMRO2 through temperature-dependent mechanisms and whether the combination of etomidate and moderate hypothermia (28°C) decreased CMRO2 more than hypothermia alone. Nineteen anesthetized dogs were treated with saline, etomidate (burst- suppressive doses), etomidate with hypothermia, or hypothermia alone. Etomidate did not affect (p > 0.05) the mean arterial pressure (MAP, mm Hg) but modestly lowered the heart rate [HR; 124 ± 6 to 105 ± 14, (mean ± SEM); p < 0.05] whereas hypothermia (without or with etomidate) lowered (p < 0.05) both MAP (141 ± 4 to 116 ± 5 and 135 ± 6 to 81 ± 7) and HR (135 ± 14 to 84 ± 3 and 135 ± 10 to 69 ± 5, respectively). Etomidate administration did not result in a change (p > 0.05) in the esophageal, brain parenchymal, or subdural temperature. CMRO2 (ml/100 g/min) decreased (p < 0.05) during etomidate administration (3.2 ± 0.4 to 1.7 ± 0.2) and hypothermia (3.5 ± 0.2 to 1.1 ± 0.2), but the addition of etomidate to hypothermia did not further reduce CMRO2 in the animals (3.1 ± 0.5 to 1.3 ± 0.2) despite decreasing their brain hemispheric electrical activity from 9 ± 1 Hz to a burst-suppressive state. During hypotension (MAP 30 ± 2) induced by sodium nitroprusside and trimethaphan administration, the cerebral arteriovenous difference in O2 (AVDO2) increased (p < 0.05) in the saline group (5.4 ± 0.9 to 10.7 ± 1.0 ml/dl) but not in the other groups. Thus, etomidate does not have adverse cardiovascular effects associated with moderate hypothermia, and decreases CMRO2 independently of brain temperature changes. Etomidate, however, in this model does not further reduce CMRO2 in moderately hypothermic animals despite decreasing their brain hemispheric electrical activity. Etomidate, hypothermia, and the combination of etomidate and hypothermia all blunt the hypotension-induced increase in cerebral AVDO2.",
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T1 - Effects of etomidate and hypothermia on cerebral metabolism and blood flow in a canine model of hypoperfusion

AU - Frizzell, R. T.

AU - Fichtel, F. M.

AU - Jordan, M. B.

AU - Weprin, B. E.

AU - Borchers, D. J.

AU - Allen, E. C.

AU - Pogue, W. R.

AU - Batjer, H. H.

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N2 - Etomidate is a nonbarbiturate hypnotic agent which, like the barbiturates, decreases the cerebral metabolic rate of oxygen consumption (CMRO2) 35-50%. The present studies assessed whether etomidate decreased CMRO2 through temperature-dependent mechanisms and whether the combination of etomidate and moderate hypothermia (28°C) decreased CMRO2 more than hypothermia alone. Nineteen anesthetized dogs were treated with saline, etomidate (burst- suppressive doses), etomidate with hypothermia, or hypothermia alone. Etomidate did not affect (p > 0.05) the mean arterial pressure (MAP, mm Hg) but modestly lowered the heart rate [HR; 124 ± 6 to 105 ± 14, (mean ± SEM); p < 0.05] whereas hypothermia (without or with etomidate) lowered (p < 0.05) both MAP (141 ± 4 to 116 ± 5 and 135 ± 6 to 81 ± 7) and HR (135 ± 14 to 84 ± 3 and 135 ± 10 to 69 ± 5, respectively). Etomidate administration did not result in a change (p > 0.05) in the esophageal, brain parenchymal, or subdural temperature. CMRO2 (ml/100 g/min) decreased (p < 0.05) during etomidate administration (3.2 ± 0.4 to 1.7 ± 0.2) and hypothermia (3.5 ± 0.2 to 1.1 ± 0.2), but the addition of etomidate to hypothermia did not further reduce CMRO2 in the animals (3.1 ± 0.5 to 1.3 ± 0.2) despite decreasing their brain hemispheric electrical activity from 9 ± 1 Hz to a burst-suppressive state. During hypotension (MAP 30 ± 2) induced by sodium nitroprusside and trimethaphan administration, the cerebral arteriovenous difference in O2 (AVDO2) increased (p < 0.05) in the saline group (5.4 ± 0.9 to 10.7 ± 1.0 ml/dl) but not in the other groups. Thus, etomidate does not have adverse cardiovascular effects associated with moderate hypothermia, and decreases CMRO2 independently of brain temperature changes. Etomidate, however, in this model does not further reduce CMRO2 in moderately hypothermic animals despite decreasing their brain hemispheric electrical activity. Etomidate, hypothermia, and the combination of etomidate and hypothermia all blunt the hypotension-induced increase in cerebral AVDO2.

AB - Etomidate is a nonbarbiturate hypnotic agent which, like the barbiturates, decreases the cerebral metabolic rate of oxygen consumption (CMRO2) 35-50%. The present studies assessed whether etomidate decreased CMRO2 through temperature-dependent mechanisms and whether the combination of etomidate and moderate hypothermia (28°C) decreased CMRO2 more than hypothermia alone. Nineteen anesthetized dogs were treated with saline, etomidate (burst- suppressive doses), etomidate with hypothermia, or hypothermia alone. Etomidate did not affect (p > 0.05) the mean arterial pressure (MAP, mm Hg) but modestly lowered the heart rate [HR; 124 ± 6 to 105 ± 14, (mean ± SEM); p < 0.05] whereas hypothermia (without or with etomidate) lowered (p < 0.05) both MAP (141 ± 4 to 116 ± 5 and 135 ± 6 to 81 ± 7) and HR (135 ± 14 to 84 ± 3 and 135 ± 10 to 69 ± 5, respectively). Etomidate administration did not result in a change (p > 0.05) in the esophageal, brain parenchymal, or subdural temperature. CMRO2 (ml/100 g/min) decreased (p < 0.05) during etomidate administration (3.2 ± 0.4 to 1.7 ± 0.2) and hypothermia (3.5 ± 0.2 to 1.1 ± 0.2), but the addition of etomidate to hypothermia did not further reduce CMRO2 in the animals (3.1 ± 0.5 to 1.3 ± 0.2) despite decreasing their brain hemispheric electrical activity from 9 ± 1 Hz to a burst-suppressive state. During hypotension (MAP 30 ± 2) induced by sodium nitroprusside and trimethaphan administration, the cerebral arteriovenous difference in O2 (AVDO2) increased (p < 0.05) in the saline group (5.4 ± 0.9 to 10.7 ± 1.0 ml/dl) but not in the other groups. Thus, etomidate does not have adverse cardiovascular effects associated with moderate hypothermia, and decreases CMRO2 independently of brain temperature changes. Etomidate, however, in this model does not further reduce CMRO2 in moderately hypothermic animals despite decreasing their brain hemispheric electrical activity. Etomidate, hypothermia, and the combination of etomidate and hypothermia all blunt the hypotension-induced increase in cerebral AVDO2.

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