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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

Puccio, Ava M (2008) Effect of Short Periods of Normobaric Hyperoxia on Local Brain Tissue Oxygenation & Cerebrospinal Fluid Oxidative Stress Markers in Severe Traumatic Brain Injury. Doctoral Dissertation, University of Pittsburgh. (Unpublished)

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Preliminary evidence suggests that PbtO2 values of ¡Ü 15 mm Hg may be suggestive of brain tissue hypoxia. Accordingly, many neurotrauma intensive care units attempt to maintain the PbtO2 ¡Ý 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¡À1.8 yrs], with severe TBI (Glasgow Coma Scale score 6¡À1.4) 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), PbtO2, arterial oxygen content (pO2)] were assessed at the same time points, using a 30 minute average prior to each FiO2 change. Mean (¡ÀSD) PbtO2 and PaO2 levels significantly changed for each time point, [before 27.3¡À7.4, 173.1¡À51.4; during 93.9¡À58.1, 385.5¡À108.3; and after 29.3¡À13.0, 171.8¡À45.1] 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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Item Type: University of Pittsburgh ETD
Status: Unpublished
CreatorsEmailPitt UsernameORCID
Puccio, Ava Mpuccioam@upmc.eduAPUCCIO
ETD Committee:
TitleMemberEmail AddressPitt UsernameORCID
Committee ChairHoffman, Leslie Alhof@pitt.eduLHOF
Committee MemberKochanek, Patrick
Committee MemberAlexander, Sheilasalexand@pitt.eduSALEXAND
Committee MemberZullo, Thomas Gzullo@pitt.eduZULLO
Committee MemberConley, Yvette Pyconley@pitt.eduYCONLEY
Date: 12 May 2008
Date Type: Completion
Defense Date: 31 March 2008
Approval Date: 12 May 2008
Submission Date: 23 April 2008
Access Restriction: No restriction; Release the ETD for access worldwide immediately.
Institution: University of Pittsburgh
Schools and Programs: School of Nursing > Nursing
Degree: PhD - Doctor of Philosophy
Thesis Type: Doctoral Dissertation
Refereed: Yes
Uncontrolled Keywords: antioxidant reserve; traumatic brain injury; normobaric hyperoxia; oxidative stress
Other ID:, etd-04232008-101618
Date Deposited: 10 Nov 2011 19:41
Last Modified: 19 Dec 2016 14:35


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