Oxygen Toxicity

Stogner, Steven W.; Payne, D. Keith

doi:10.1177/106002809202601214

Cited by 42 publications

(30 citation statements)

References 55 publications

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“…The pathogenesis of damage induced by hyperoxia in the lung is not well understood, but it is believed to be mediated by direct damage to the cell through the generation of ROS [40]. Hyperoxia causes cell injury presumably because cellular antioxidant defenses become overwhelmed [41], leading to the accumulation of toxic levels of ROS. The components of ROS include O − 2 , H 2 O 2 , and HOCl [12], and the oxidative burden they create can reduce the levels of antioxidant enzymes [33].…”

Section: Discussionmentioning

confidence: 99%

Hyperoxia-Induced Lung Injury Is Dose Dependent in Wistar Rats

Nagato¹,

Silva²,

Silva³

et al. 2009

Experimental Lung Research

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Oxygen is indispensable for aerobic respiration. However, the effects of hyperoxia on the lungs are poorly defined. The aim of the present study was to determine the effects of different oxygen concentrations on rat lungs. Rats (n = 6 per group) were exposed to hyperoxia for 90 minutes at 3 different concentrations: 50% (H50%), 75% (H75%), or 100% (H100%). Bronchoalveolar lavage (BAL) was performed and the right lungs were removed for histological analyses. The BAL samples were assayed for lipid peroxidation and antioxidant status using biochemical methods. Hyperoxia induced influxes of macrophages (1.8- to 2.3-fold) and neutrophils (7.0- to 10.2-fold) into the lungs compared to the control group (exposed to normoxia; n = 6). Histological analyses of the hyperoxic groups showed hemorrhagic areas and septal edema. A significant increase (2.2-fold) in lipid peroxidation was observed in the H100% group compared to the control group (P <.05). Glutathione peroxidase and superoxide dismutase activities were reduced to approximately 20% and 40% of the control values, respectively, in all 3 hyperoxic groups, and catalase activity was reduced in both the H75% (-0.6-fold) and H100% (-0.7-fold) groups. These results indicate a harmful effect of hyperoxia on the rat lung, with evidence of oxidant/antioxidant imbalance and histological damage.

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Section: Discussionmentioning

confidence: 99%

Hyperoxia-Induced Lung Injury Is Dose Dependent in Wistar Rats

Nagato¹,

Silva²,

Silva³

et al. 2009

Experimental Lung Research

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“…Pure oxygen at atmospheric pressure is safe if given for less than 6 h [35] and the first morphological changes in rat lungs exposed to 100% oxygen develop only after 40 h of continuous exposure [36], far beyond 1 h/d exposure, which was used in the present study. The main complication of brief periods of oxygen administration is pulmonary atelectasis [34] and preoxygenation with 80% oxygen is associated with considerably lower rates of atelectasis compared with 100% oxygen [37].…”

Section: Discussionmentioning

confidence: 99%

Preconditioning With Oxygen Attenuates Rat Renal Ischemia–Reperfusion Injury

Rasoulian

Mohammadhosseniakbari

Kadkhodaee

et al. 2008

Journal of Surgical Research

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“…Oxygen, as well as reactive oxygen species generated in high O 2 , can modulate many physiological and pathological signaling pathways (27). This is especially true for pathways involving heme proteins (28).…”

Section: Discussionmentioning

confidence: 99%

Oxygen modulation of neurovascular coupling in the retina

Mishra

Hamid

Newman

2011

Proc. Natl. Acad. Sci. U.S.A.

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Neurovascular coupling is a process through which neuronal activity leads to local increases in blood flow in the central nervous system. In brain slices, 100% O 2 has been shown to alter neurovascular coupling, suppressing activity-dependent vasodilation. However, in vivo, hyperoxia reportedly has no effect on blood flow. Resolving these conflicting findings is important, given that hyperoxia is often used in the clinic in the treatment of both adults and neonates, and a reduction in neurovascular coupling could deprive active neurons of adequate nutrients. Here we address this issue by examining neurovascular coupling in both ex vivo and in vivo rat retina preparations. In the ex vivo retina, 100% O 2 reduced light-evoked arteriole vasodilations by 3.9-fold and increased vasoconstrictions by 2.6-fold. In vivo, however, hyperoxia had no effect on light-evoked arteriole dilations or blood velocity. Oxygen electrode measurements showed that 100% O 2 raised pO 2 in the ex vivo retina from 34 to 548 mm Hg, whereas hyperoxia has been reported to increase retinal pO 2 in vivo to only ∼53 mm Hg [Yu DY, Cringle SJ, Alder VA, Su EN (1994) Am J Physiol 267:H2498-H2507]. Replicating the hyperoxic in vivo pO 2 of 53 mm Hg in the ex vivo retina did not alter vasomotor responses, indicating that although O 2 can modulate neurovascular coupling when raised sufficiently high, the hyperoxia-induced rise in retinal pO 2 in vivo is not sufficient to produce a modulatory effect. Our findings demonstrate that hyperoxia does not alter neurovascular coupling in vivo, ensuring that active neurons receive an adequate supply of nutrients.functional hyperemia | glial cells | prostaglandins N euronal activity in the CNS induces local increases in blood flow (1, 2), a homeostatic response termed functional hyperemia. Neurovascular coupling, the process mediating this response, is thought to involve signaling from neurons to glial cells to blood vessels. Neuronal activity induces a rise in intracellular Ca 2+ in glial cell endfeet surrounding vessels, leading to the release of vasoactive arachidonic acid metabolites and resulting in vasomotor responses (2-6). Experiments in brain slices and in the ex vivo retina have revealed that glial activation can evoke both vasodilation and vasoconstriction. Evoked vasodilations are mediated by cyclooxygenase (COX) products (3, 5) and epoxyeicosatrienoic acids (EETs) (6-9), whereas vasoconstrictions are mediated by 20-hydroxyeicosatetraenoic acid (20-HETE) (4,6).A recent study demonstrated that neurovascular coupling is modulated by O 2 in brain slices (10). Both neuronal and glial cell stimulation elicited vasodilations in brain slices exposed to 20% O 2 . In contrast, vasoconstrictions were evoked in the presence of 100% O 2 . However, another recent study reported the opposite effect of O 2 in vivo (11). In that study, increasing systemic O 2 using hyperbaric hyperoxygenation had no effect on cortical functional hyperemia. Resolving these conflicting findings is critical, given that hyperoxia (breat...

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Oxygen Toxicity

Cited by 42 publications

References 55 publications

Hyperoxia-Induced Lung Injury Is Dose Dependent in Wistar Rats

Hyperoxia-Induced Lung Injury Is Dose Dependent in Wistar Rats

Preconditioning With Oxygen Attenuates Rat Renal Ischemia–Reperfusion Injury

Oxygen modulation of neurovascular coupling in the retina

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