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Effect of short periods of normobaric hyperoxia on local brain tissue oxygenation & cerebrospinal fluid oxidative stress markers in severe traumatic brain injury.

Record Type:	Language materials, printed : Monograph/item
Title/Author:	Effect of short periods of normobaric hyperoxia on local brain tissue oxygenation & cerebrospinal fluid oxidative stress markers in severe traumatic brain injury./
Author:	Puccio, Ava M.
Description:	88 p.
Notes:	Source: Dissertation Abstracts International, Volume: 69-07, Section: B, page: 4078.
Contained By:	Dissertation Abstracts International69-07B.
Subject:	Biology, Neuroscience. -
Online resource:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3322359
ISBN:	9780549732600

Effect of short periods of normobaric hyperoxia on local brain tissue oxygenation & cerebrospinal fluid oxidative stress markers in severe traumatic brain injury.
Puccio, Ava M.

Effect of short periods of normobaric hyperoxia on local brain tissue oxygenation & cerebrospinal fluid oxidative stress markers in severe traumatic brain injury. - 88 p.

Source: Dissertation Abstracts International, Volume: 69-07, Section: B, page: 4078.

Thesis (Ph.D.)--University of Pittsburgh, 2008.

Preliminary evidence suggests that PbtO2 values of ≤ 15 mm Hg may be suggestive of brain tissue hypoxia. Accordingly, many neurotrauma intensive care units attempt to maintain the PbtO2 ≥ 20 mm Hg based on the belief that this intervention will increase availability of oxygen in the brain for metabolism, and will avoid periods of brain tissue hypoxia with a 5 mm Hg buffer range. In clinical practice, one approach to managing a low PbtO2 (< 20 torr) is to increase the delivered fraction of inspired oxygen (FiO2). It remains unclear whether this therapy has risks as it also has the potential to increase oxidative stress. To determine if short periods of normobaric hyperoxia (2h) affect oxidative stress markers and antioxidant defenses, cerebrospinal fluid (CSF) was assessed in adults [n=11, (9 male, 2 female), mean age 26+/-1.8 yrs], with severe TBI (Glasgow Coma Scale score 6+/-1.4) before, during, and after a FiO2=1.0 challenge. Markers of oxidative stress including lipid peroxidation (F2-isoprostane [ELISA]) and protein oxidation (protein sulfhydryls [fluorescence]) and markers of antioxidant defenses including total antioxidant reserve (AOR) [chemiluminescence] and glutathione [fluorescence] were evaluated in CSF. Physiological parameters, [intracranial pressure (ICP), mean arterial pressure (MAP), cerebral perfusion pressure (CPP), PbtO 2, arterial oxygen content (pO2)] were assessed at the same time points, using a 30 minute average prior to each FiO2 change. Mean (+/-SD) PbtO2 and PaO2 levels significantly changed for each time point, [before 27.3+/-7.4, 173.1+/-51.4; during 93.9+/-58.1, 385.5+/-108.3; and after 29.3+/-13.0, 171.8+/-45.1] a FiO2 challenge, (p=.04; .01), respectively. Oxidative stress markers, antioxidant reserve defenses and physiological parameters did not significantly change for any time period. These preliminary findings suggest that brief periods of normobaric hyperoxia improve oxygen levels without producing local oxidative stress in brain tissue. Additional studies are required to examine extended periods of normobaric hyperoxia and application of treatment during periods of critical PbtO2 levels.

ISBN: 9780549732600Subjects--Topical Terms:

1017680
Biology, Neuroscience.

Effect of short periods of normobaric hyperoxia on local brain tissue oxygenation & cerebrospinal fluid oxidative stress markers in severe traumatic brain injury.
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245 1 0 $a Effect of short periods of normobaric hyperoxia on local brain tissue oxygenation & cerebrospinal fluid oxidative stress markers in severe traumatic brain injury.
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500 $a Source: Dissertation Abstracts International, Volume: 69-07, Section: B, page: 4078.
502 $a Thesis (Ph.D.)--University of Pittsburgh, 2008.
520 $a Preliminary evidence suggests that PbtO2 values of ≤ 15 mm Hg may be suggestive of brain tissue hypoxia. Accordingly, many neurotrauma intensive care units attempt to maintain the PbtO2 ≥ 20 mm Hg based on the belief that this intervention will increase availability of oxygen in the brain for metabolism, and will avoid periods of brain tissue hypoxia with a 5 mm Hg buffer range. In clinical practice, one approach to managing a low PbtO2 (< 20 torr) is to increase the delivered fraction of inspired oxygen (FiO2). It remains unclear whether this therapy has risks as it also has the potential to increase oxidative stress. To determine if short periods of normobaric hyperoxia (2h) affect oxidative stress markers and antioxidant defenses, cerebrospinal fluid (CSF) was assessed in adults [n=11, (9 male, 2 female), mean age 26+/-1.8 yrs], with severe TBI (Glasgow Coma Scale score 6+/-1.4) before, during, and after a FiO2=1.0 challenge. Markers of oxidative stress including lipid peroxidation (F2-isoprostane [ELISA]) and protein oxidation (protein sulfhydryls [fluorescence]) and markers of antioxidant defenses including total antioxidant reserve (AOR) [chemiluminescence] and glutathione [fluorescence] were evaluated in CSF. Physiological parameters, [intracranial pressure (ICP), mean arterial pressure (MAP), cerebral perfusion pressure (CPP), PbtO 2, arterial oxygen content (pO2)] were assessed at the same time points, using a 30 minute average prior to each FiO2 change. Mean (+/-SD) PbtO2 and PaO2 levels significantly changed for each time point, [before 27.3+/-7.4, 173.1+/-51.4; during 93.9+/-58.1, 385.5+/-108.3; and after 29.3+/-13.0, 171.8+/-45.1] a FiO2 challenge, (p=.04; .01), respectively. Oxidative stress markers, antioxidant reserve defenses and physiological parameters did not significantly change for any time period. These preliminary findings suggest that brief periods of normobaric hyperoxia improve oxygen levels without producing local oxidative stress in brain tissue. Additional studies are required to examine extended periods of normobaric hyperoxia and application of treatment during periods of critical PbtO2 levels.
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