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Query: UMLS:C0242706 (hyperoxia)
 5,219 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To investigate the pathogenesis of oxygen toxicity in the newborn brain, we exposed one-day-old Sprague-Dawley albino rats to 100% O(2) and measured whole-brain high-energy phosphates, glucose, lactate, and free fatty acids (FFA) after 0, 15, 30, 60 and 120 min. Whole-brain adenosine triphosphate and creatine phosphate fell significantly from about 4.5 to 2.5 ?mol-mg(?1) protein. Brain lactate remained at about 0.3 ?mol.mg(?1) protein in hyperoxic rats, but increased in normoxic rats, from 0.3 to 1.3 ?mol.mg(?1) protein at 120 min. Total FFA decreased from 30 to 15 nmol.mg(?1) protein during normoxia, but increased to 40 nmol.mg(?1) protein during hyperoxia. Undetectable in normoxic rats, arachidonic acid increased to between 4 and 6 nmol.mg(?1) protein during hyperoxia while oleic acid increased by two to threefold. In normoxia, palmitate decreased by 70% from 12 to 4 nmol.mg(?1) protein whereas in hyperoxia it remained at 10 nmol.mg(?1) protein. Normobaric 100% O(2) has detrimental metabolic effects on the neonatal brain which cannot be attributed to cerebral vasospasm or seizure-induced cerebral anoxia because lactic acidosis was not observed. FFA changes suggest that a likely explanation is membrane lipid peroxidation from O(2)-induced free radicals.
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PMID:Detrimental cerebrometabolic effects of hyperoxia in newborn rats. 2050 Nov 6

The development of cerebral vasospasm in subarachnoid hemorrhage (SAH) due to cerebral aneurysms rupture results in cerebral circulation disturbances. Application of normobaric hyperoxia can be an effective way for improving of oxygen delivery to injured brain tissues. The purpose of this study was to assess of normobaric hyperoxia influence on intracranial pressure (ICP), cerebral oxygenation and metabolism, oxidative stress and endogenous factors of vascular regulation in II critically ill patients with nontraumatic SAH due to cerebral aneurysms rupture. Increase of FiO2 from 0.3 to 0.5 and 1.0 was accompanied with brain oxygen tension (PbrO2) increase and cerebral extraction ratio for oxygen (O2ER) decrease. Application of normobaric hyperoxia had no effect on ICP, cerebral perfusion pressure, arterial blood pressure and cerebral metabolism. The results obtained from patients with nontraumatic SAH showed an evident increase of oxidative stress which had a significant effect on vascular endothelial function, causing an imbalance in the endogenous regulation of vascular tone. Application of normobaric hyperoxia was not accompanied by an increase of free-radical processes in critically ill patients with nontraumatic SAH due to cerebral aneurysms rupture.
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PMID:[Effect of normobaric hyperoxia on cerebral oxygenation, metabolism and oxidative stress in patients with subarachnoid hemorrhage caused by intracranial aneurysm rupture]. 2434 Oct 47