1985
DOI: 10.1097/00000542-198510000-00005
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Cerebral Functional, Metabolic, and Hemodynamic Effects of Etomidate in Dogs

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Cited by 118 publications
(34 citation statements)
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“…This is in agreement with other centrally acting anaesthetics, since burst suppression occurs with barbiturates [3 1,321, isoflurane [18,33,34], desflurane [21], etomidate [35] and propofol [23]. With regard to anaesthetic depth, burst suppression does not reliably indicate a deep or adequate anaesthetic state; nor does it prevent reactions to noxious stimuli such as laryngoscopy and intubation [24,37].…”
Section: Discussionsupporting
confidence: 72%
“…This is in agreement with other centrally acting anaesthetics, since burst suppression occurs with barbiturates [3 1,321, isoflurane [18,33,34], desflurane [21], etomidate [35] and propofol [23]. With regard to anaesthetic depth, burst suppression does not reliably indicate a deep or adequate anaesthetic state; nor does it prevent reactions to noxious stimuli such as laryngoscopy and intubation [24,37].…”
Section: Discussionsupporting
confidence: 72%
“…The different effects of iv anesthetics on oxygen saturation may be due to the different actions on cerebral blood flow and oxygen consumption; both propofol and thiopental maintain flow-metabolism coupling 12 whereas etomidate is associated with a rapid reduction in cerebral blood flow accompanied by a slower reduction in oxygen consumption. 13 Iwasaki et al 14 compared the effects of higher doses of sevoflurane (8%) on cerebral blood volume with 5% sevoflurane and propofol on cerebral volume using BIS and NIRS during induction of anesthesia. Only vital capacity inhalation with 8% sevoflurane produced an increase in cerebral blood volume, suggesting that high concentrations of sevoflurane may be dangerous in patients with elevated intracranial pressure.…”
Section: Discussionmentioning
confidence: 99%
“…The later result can exist because low concentration of phytoestrogens might not be adequate to fully activate the neuroprotective pathways [19] for prohibiting ICP elevation on days post-TBI. The causes of the ICP increase in TBI could be hypoxia [45], the reduction of cerebral blood flow [46], cerebral edema [47], ischemic injury, hyper-perfusion in the early stages after TBI [48], changes in the expression of aquaporin-4 [49] and vaso-paralysis, and impaired auto-regulation [50]. It seems that our study is the first to evaluate the effect of soy on ICP.…”
Section: Discussionmentioning
confidence: 99%