Details

Autor(en) / Beteiligte

• Vidal-Jorge, Marian
• Sánchez-Guerrero, Angela
• Mur-Bonet, Gemma
• Castro, Lidia
• Rădoi, Andreea
• Riveiro, Marilyn
• Fernández-Prado, Natalia
• Baena, Jacinto
• Poca, Maria-Antonia
• Sahuquillo, Juan

Titel

Does Normobaric Hyperoxia Cause Oxidative Stress in the Injured Brain? A Microdialysis Study Using 8-Iso-Prostaglandin F2α as a Biomarker

Ist Teil von

• Journal of neurotrauma, 2017-10, Vol.34 (19), p.2731-2742

Ort / Verlag

United States

Erscheinungsjahr

2017

Quelle

MEDLINE

Beschreibungen/Notizen

• Significant controversy exists regarding the potential clinical benefit of normobaric hyperoxia (NBO) in patients with traumatic brain injury (TBI). This study consisted of two aims: 1) to assess whether NBO improves brain oxygenation and metabolism and 2) to determine whether this therapy may increase the risk of oxidative stress (OxS), using 8-iso-Prostaglandin F2α (PGF2α) as a biomarker. Thirty-one patients with a median admission Glasgow Coma Scale score of 4 (min: 3, max: 12) were monitored with cerebral microdialysis and brain tissue oxygen sensors and treated with fraction of inspired oxygen (FiO ) of 1.0 for 4 h. Patients were divided into two groups according to the area monitored by the probes: normal injured brain and traumatic penumbra/traumatic core. NBO maintained for 4 h did not induce OxS in patients without preOxS at baseline, except in one case. However, for patients in whom OxS was detected at baseline, NBO induced a significant increase in 8-iso-PGF2α. The results of our study showed that NBO did not change energy metabolism in the whole group of patients. In the five patients with brain lactate concentration ([Lac] ) > 3.5 mmol/L at baseline, NBO induced a marked reduction in both [Lac] and lactate-to-pyruvate ratio. Although these differences were not statistically significant, together with the results of our previous study, they suggest that TBI patients would benefit from receiving NBO when they show indications of disturbed brain metabolism. These findings, in combination with increasing evidence that TBI metabolic crises are common without brain ischemia, open new possibilities for the use of this accessible therapeutic strategy in TBI patients.