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Journal ArticleDOI

Impact of anesthetic agents on cerebrovascular physiology in children.

01 Feb 2009-Pediatric Anesthesia (Blackwell Publishing Ltd)-Vol. 19, Iss: 2, pp 108-118
TL;DR: The understanding of the effects of anesthetic agents on the physiology of cerebral vasculature in the pediatric population has significantly increased in the past decade allowing a more rationale decision making in anesthesia management.
Abstract: care to children with neurologic pathologies. The cerebral physiology is influenced by the developmental stage of the child. The understanding of the effects of anesthetic agents on the physiology of cerebral vasculature in the pediatric population has significantly increased in the past decade allowing a more rationale decision making in anesthesia management. Although no single anesthetic technique can be recommended, sound knowledge of the principles of cerebral physiology and anesthetic neuropharmacology will facilitate the care of pediatric neurosurgical patients.

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TL;DR: There is no direct evidence in humans for propofol-induced neurotoxicity to the infant brain; however, current concerns of neuroapoptosis in developing brains induced by prop ofol persist and continue to be a focus of research.
Abstract: Propofol is an intravenous agent used commonly for the induction and maintenance of anesthesia, procedural, and critical care sedation in children. The mechanisms of action on the central nervous system involve interactions at various neurotransmitter receptors, especially the gamma-aminobutyric acid A receptor. Approved for use in the USA by the Food and Drug Administration in 1989, its use for induction of anesthesia in children less than 3 years of age still remains off-label. Despite its wide use in pediatric anesthesia, there is conflicting literature about its safety and serious adverse effects in particular subsets of children. Particularly as children are not “little adults”, in this review, we emphasize the maturational aspects of propofol pharmacokinetics. Despite the myriad of propofol pharmacokinetic-pharmacodynamic studies and the ability to use allometrical scaling to smooth out differences due to size and age, there is no optimal model that can be used in target controlled infusion pumps for providing closed loop total intravenous anesthesia in children. As the commercial formulation of propofol is a nutrient-rich emulsion, the risk for bacterial contamination exists despite the Food and Drug Administration mandating addition of antimicrobial preservative, calling for manufacturers’ directions to discard open vials after 6 h. While propofol has advantages over inhalation anesthesia such as less postoperative nausea and emergence delirium in children, pain on injection remains a problem even with newer formulations. Propofol is known to depress mitochondrial function by its action as an uncoupling agent in oxidative phosphorylation. This has implications for children with mitochondrial diseases and the occurrence of propofol-related infusion syndrome, a rare but seriously life-threatening complication of propofol. At the time of this review, there is no direct evidence in humans for propofol-induced neurotoxicity to the infant brain; however, current concerns of neuroapoptosis in developing brains induced by propofol persist and continue to be a focus of research.

256 citations


Cites background from "Impact of anesthetic agents on cere..."

  • ...This is associated with a fall in cerebral blood flow, metabolic demand for oxygen, and any pre-existing cerebral edema [88, 89]....

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Journal ArticleDOI
TL;DR: Near‐infrared spectroscopy provides noninvasive continuous access to the venous side of regional circulations that can approximate organ‐specific and global measures to facilitate the detection of circulatory abnormalities and drive goal‐directed interventions to reduce end‐organ ischemic injury.
Abstract: The safety of anesthesia has improved greatly in the past three decades. Standard perioperative monitoring, including pulse oximetry, has practically eliminated unrecognized arterial hypoxia as a cause for perioperative injury. However, most anesthesia-related cardiac arrests in children are now cardiovascular in origin, and standard monitoring is unable to detect many circulatory abnormalities. Near-infrared spectroscopy provides noninvasive continuous access to the venous side of regional circulations that can approximate organ-specific and global measures to facilitate the detection of circulatory abnormalities and drive goal-directed interventions to reduce end-organ ischemic injury.

96 citations

Journal ArticleDOI
TL;DR: The advantages of total intravenous anesthesia (TIVA) have emerged and driven change in practice as mentioned in this paper, and these advantages will justify why TIVA will supercede inhalational anesthesia in future pediatric anesthetic practice.
Abstract: Inhalational anesthesia has dominated the practice of pediatric anesthesia. However, as the introduction of agents such as propofol, short-acting opioids, midazolam, and dexmedetomidine a monumental change has occurred. With increasing use, the overwhelming advantages of total intravenous anesthesia (TIVA) have emerged and driven change in practice. These advantages, outlined in this review, will justify why TIVA will supercede inhalational anesthesia in future pediatric anesthetic practice.

72 citations

01 Jan 1995
TL;DR: In this paper, the effects of a high affinity gamma-aminobutyric acid (GABA)-benzodiazepine-receptor agonist (lorazepam) and an antagonist (flumazenil) in humans, using H2(15)O positron-emission tomography were studied.
Abstract: We studied the effects of a high-affinity gamma-aminobutyric acid (GABA)-benzodiazepine-receptor agonist (lorazepam) and an antagonist (flumazenil) in humans, using H2(15)O positron-emission tomography. Administration of lorazepam to healthy volunteers caused time- and dose-dependent reductions in regional cerebral blood flow and self-reported alterations in behavioral/mood parameters. Flumazenil administration reversed these changes. These observations indicated that benzodiazepine-induced effects on regional cerebral blood flow and mood/behavior are mediated at some level through GABA-benzodiazepine receptors, although the specific mechanism remains unclear. The approach described here provides a method for quantifying GABA-benzodiazepine-receptor-mediated neurotransmission in the living human brain and may be useful for studying the role of these receptors in a variety of neuropsychiatric disorders.

53 citations

References
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Journal ArticleDOI
TL;DR: The uneven change in distribution of the CBF when N2O was added during hypocapnia, the reduced carbon dioxide response, and the lack of effect of N1O on isolated human pial arteries suggest that N2 O may increase metabolism in selected brain areas.
Abstract: BACKGROUND: Results from previous studies on the effect of nitrous oxide (N2O) on the cerebral circulation are conflicting. Early reports claim N2O to have no effect whereas recent findings demonstrate a cerebral cortical vasodilatation during N2O inhalation, but the regional cerebral blood flow (CBF) in the subcortical structures is unknown. METHODS: Regional CBF was measured three-dimensionally with single photon emission computer-aided tomography after injection of xenon 133 in 8 spontaneously breathing men (mean age 29.6 yr) during normocapnia and hypocapnia with and without inhalation of 50% N2O. 8 isolated human pial arterial segments were mounted in organ baths. The segments were contracted with prostaglandin F2 alpha and subjected to 30% oxygen and 5.6% carbon dioxide in nitrogen or N2O. RESULTS: Normocapnic young men had a global CBF of 55 +/- 4 ml.100 g-1.min-1. Decreasing end-tidal CO2 tension by 1.3 kPa (9.3 mmHg) reduced CBF uniformly, with a decrease in global CBF to 45 +/- 2 ml.100 g-1.min-1 (P < 0.0001). During normocapnia, inhalation of 50% N2O increased mean CBF to 67 +/- 7 ml.100 g-1.min-1 (P < 0.0001). Inhalation of 50% N2O during hypocapnia increased mean CBF to 63 +/- 5 ml.100 g-1.min-1 (P < 0.0001). During N2O inhalation there was no significant difference in mean CBF between normo- and hypocapnia. However, during hypocapnia, but not during normocapnia, N2O inhalation significantly changed the distribution of regional CBF (P < 0.0001). Compared with hypocapnia without N2O, flow increased through the frontal (143%), parietal (140%) and temporal (133%) regions as well as through insula (151%), basal ganglia (145%) and thalamus (133%). In isolated human pial arteries, addition of N2O changed neither basal tension, nor the contraction elicited by prostaglandin F2 alpha. CONCLUSIONS: Inhalation of 50% N2O increased global CBF mainly by augmenting flow in frontal brain structures. In contrast, changes in carbon dioxide without N2O affected CBF uniformly in the brain. The uneven change in distribution of the CBF when N2O was added during hypocapnia, the reduced carbon dioxide response, and the lack of effect of N2O on isolated human pial arteries suggest that N2O may increase metabolism in selected brain areas. (Less)

66 citations

Journal ArticleDOI
TL;DR: The results suggest that tissue hypoxia and acidosis are often observed during etomidate treatment and middle cerebral artery occlusion, and treatment with desflurane significantly increases tissue P (O)2 alone and attenuates acidotic changes to prolongedmiddle cerebral artery Occlusion.
Abstract: Background: The authors compared the effects of etomidate and desflurane on brain tissue oxygen pressure (Po 2 ), carbon dioxide pressure (Pco 2 ), and pH in patients who had middle cerebral artery occlusion for >15 min. Methods: After a craniotomy, a probe that measures Po 2 , Pco 2 and pH was inserted into cortical tissue at risk for ischemia during middle cerebral artery occlusion. A burst suppression pattern of the electroencephalogram was induced with etomidate (n = 6) or 9% end-tidal desflurane (n = 6) started before middle cerebral artery occlusion. Mean blood pressure was supported with phenylephrine to 90-95 mmHg. Results: During baseline conditions, tissue Po 2 , Pco 2 , and pH were similar between the two groups (Po 2 = 15 mmHg, Pco 2 = 60 mmHg,pH = 7.1). During administration of etomidate before middle cerebral artery occlusion, tissue Po 2 decreased in five of six patients without a change in Pco 2 or pH. During administration of 9% desflurane, tissue Po 2 and pH increased before middle cerebral artery clipping. Middle cerebral artery occlusion for an average of 33 min with etomidate and 37 min with desflurane produced a decrease in pH with etomidate (7.09 to 6.63, P < 0.05) but not with desflurane (7.12 to 7.15). Conclusion: These results suggest that tissue hypoxia and acidosis are often observed during etomidate treatment and middle cerebral artery occlusion. Treatment with desflurane significantly increases tissue Po 2 alone and attenuates acidotic changes to prolonged middle cerebral artery occlusion.

63 citations

Journal ArticleDOI
TL;DR: Subjects who received diazepam showed marked right hemispheric rCBF decreases, especially in the frontal lobe, whereas controls did not show significant differences between the two sets of values.

62 citations

Journal ArticleDOI
TL;DR: It is concluded that nitrous oxide, when added to isoflurane concentrations ranging from 1.4% to 3.5% in the dog, increases CBF at the low but not the high isolectric concentrations although it has no effect on CMRo2.
Abstract: The purpose of this canine study was to examine the cerebral vascular and metabolic effects of adding nitrous oxide to isoflurane from 1.4% expired (1 MAC) up to a concentration giving an isoelectric electroencephalogram (EEG). Cerebral blood flow (CBF) and cerebral metabolic rate for oxygen (CMRO2) were determined using a sagittal sinus outflow technique. At 1.4% expired isoflurane, 70% nitrous oxide increased CBF but had no effect on CMRO2. At 3.1% expired isoflurane, 70% nitrous oxide had no effect on either CBF or CMRO2. The latter concentration of isoflurane rendered the EEG isoelectric, but when nitrous oxide was added, EEG activity reappeared. To again produce an isoelectric EEG required an increase in the isoflurane concentration to 3.5% +/- 0.2% (with no further effect on CMRO2). The authors also found that at 1.4% isoflurane, 0.9 micrograms.kg-1.min-1 of angiotensin significantly decreased CMRO2 without any effect on CBF. It is concluded that nitrous oxide, when added to isoflurane concentrations ranging from 1.4% to 3.5% in the dog, increases CBF at the low but not the high isoflurane concentrations although it has no effect on CMRO2.

60 citations