Cottrell and Young's Neuroanesthesia 2010
DOI: 10.1016/b978-0-323-05908-4.10010-7
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Effects of Anesthetic Agents and Other Drugs on Cerebral Blood Flow, Metabolism, and Intracranial Pressure

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Cited by 25 publications
(26 citation statements)
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“…Ketamine is an N-methyl-D-aspartate antagonist with proven neuroprotective effects both, in vivo (126,127), and in vitro (128)(129)(130). However, it is also a potent cerebral vasodilator producing increases in CBF, CBV, CMRO 2 and potentially ICP, and can not be recommended in patients with reduced intracranial compliance (74,(131)(132)(133).…”
Section: Intravenous Anesthetic Agentsmentioning
confidence: 99%
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“…Ketamine is an N-methyl-D-aspartate antagonist with proven neuroprotective effects both, in vivo (126,127), and in vitro (128)(129)(130). However, it is also a potent cerebral vasodilator producing increases in CBF, CBV, CMRO 2 and potentially ICP, and can not be recommended in patients with reduced intracranial compliance (74,(131)(132)(133).…”
Section: Intravenous Anesthetic Agentsmentioning
confidence: 99%
“…All potent volatile anesthetics are direct cerebral vasodilators. Halothane is widely regarded as the most potent (74). In children, halothane induced increases in CBF persist even after halothane concentrations have been decreased (75).…”
mentioning
confidence: 99%
“…But in our study the mean propofol dose requirement was 71.26 ± 11.78 µg/ kg/min for maintenance of anesthesia supplemented with butorphanol and N 2 O in neurosurgeries. Due to its unfavorable effects on cerebral hemodynamics and cerebrospinal fluid dynamics [1] and tendency to cause postoperative nausea and vomiting (PONV) [25] N 2 O has a controversial role in current day neurosurgical anesthesiology. In our study the mean maintenance and overall dose of propofol without the use of N 2 O 90.82 ± 19.13 µg/kg/min and 100.02 ± 20.28 µg/kg/min respectively.…”
Section: Discussionmentioning
confidence: 99%
“…It causes a dose dependent decrease in intracranial pressure maintaining cerebral perfusion at modest doses. Furthermore it causes a reduction in cerebral metabolic rate (CMR) without any disturbance in cerebral reactivity to carbon dioxide and autoregulation [1]. Nitrous oxide (N 2 O) is less preferred anesthetic agent in current neurosurgical anesthesiology practice due to its unfavorable effects on neurophysiology.…”
Section: Introductionmentioning
confidence: 99%
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