Oxygen Toxicity. Arterial and Internal Jugular Blood Gas Composition in Man During Inhalation of Air, 100% O2 and 2% CO2 in O2 at 3.5 Atmospheres Ambient Pressure

Lambertsen, CJ; Ewing, J. H.; Kough, R. H.; Gould, Robert A.; Stroud, Morris W.

doi:10.1152/jappl.1955.8.3.255

Cited by 84 publications

(22 citation statements)

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“…Lipid from red cells of tocopherol-deficient mice not exposed to OHP formed no pink pigment with TBA and gave a Discussion Although the clinical and histopathologic features of oxygen toxicity have been described in detail (41)(42)(43)(44)(45)(46)(47)(48)(49)(50)(51)(52), the primary mechanism of cell damage by high oxygen tensions has not been elucidated. The development and use of oxygen under high pressure in hyperbaric chambers for medical purposes have made these effects of considerable practical importance since the in vivo levels of alveolar, venous, and arterial blood oxygen tensions reached during OHP far exceed those which are achieved by any other means (53)(54)(55)(56). Aside from studies relating to erythropoiesis, the in vivo effect of increased oxygen tension on erythrocytes has received little attention.…”

Section: Methodsmentioning

confidence: 99%

Effects of in vivo hyperoxia on erythrocytes. 3. In vivo peroxidation of erythrocyte lipid.

Mengel¹,

Kann²

1966

J. Clin. Invest.

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Section: Methodsmentioning

confidence: 99%

Effects of in vivo hyperoxia on erythrocytes. 3. In vivo peroxidation of erythrocyte lipid.

Mengel¹,

Kann²

1966

J. Clin. Invest.

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“…In rats, O 2-induced seizures (i.e., CNS O2 toxicity) occur after 3-5 h at 3 ATA O2 and more rapidly at 5-6 ATA O 2 (63). Blood-gas measurements in humans show that arterial PO 2 increases from ϳ90 Torr while normobaric air is breathed to a maximum of 1,900-2,000 Torr while 100% O 2 is breathed at 3.5 ATA (45). Hyperbaric oxygen therapy typically uses Ͼ1 to 3 ATA O 2 (65).…”

Section: Hyperoxia Hypercapnia and The Rationale For Gas Levels Usedmentioning

confidence: 99%

“…Finally, "hypercapnic HBO2" describes aCSF that was both hypercapnic and hyperoxic, as defined above, and is administered to the brain stem slice at 3 ATA. In the intact animal, the addition of hypercapnia to HBO2 also increases cerebral blood flow and thus increases PtiO 2 for any given level of inspired PO2 (45,46). In the brain slice, which is devoid of blood flow, this will not occur.…”

Section: Hyperoxia Hypercapnia and The Rationale For Gas Levels Usedmentioning

confidence: 99%

“…Rats acutely exposed to 8.3% CO 2 (arterial PCO 2 ϭ 70.8 Torr), while at 3-4 ATA HBO 2 , manifest symptoms of CNS oxygen toxicity much earlier than animals at the same PO 2 not exposed to CO 2 (13). Traditionally, the effects of hypercapnia on O 2 toxicity have been attributed to CO 2 -induced vasodilation of cerebral vessels and increased delivery of hyperoxic blood to the CNS (45). The brain slice is devoid of blood flow; hence, this preparation is well suited to determine whether there is an interaction between CO 2 and HBO 2 at the cellular level.…”

Section: Co 2 -O 2 Interactionsmentioning

confidence: 99%

“…The cellular mechanism by which hyperoxia stimulates breathing is unknown; however, several possibilities have been proposed, including the Haldane effect with increased arterial PCO 2 (45) and direct stimulation of respiratory neurons and/or the central CO 2 /H ϩ chemoreceptors (17,48). In this study, we have tested three hypotheses.…”

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confidence: 96%

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Hyperbaric oxygen and chemical oxidants stimulate CO₂/H⁺-sensitive neurons in rat brain stem slices

Mulkey

Henderson²,

Putnam³

et al. 2003

Journal of Applied Physiology

153

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. Hyperbaric oxygen and chemical oxidants stimulate CO2/H ϩ -sensitive neurons in rat brain stem slices. J Appl Physiol 95: 910-921, 2003. First published April 18, 2003 10.1152/japplphysiol.00864. 2002-Hyperoxia, a model of oxidative stress, can disrupt brain stem function, presumably by an increase in O2 free radicals. Breathing hyperbaric oxygen (HBO 2) initially causes hyperoxic hyperventilation, whereas extended exposure to HBO 2 disrupts cardiorespiratory control. Presently, it is unknown how hyperoxia affects brain stem neurons. We have tested the hypothesis that hyperoxia increases excitability of neurons of the solitary complex neurons, which is an important region for cardiorespiratory control and central CO2/H ϩ chemoreception. Intracellular recordings were made in rat medullary slices during exposure to 2-3 atm of HBO 2, HBO 2 plus antioxidant (Trolox C), and chemical oxidants (N-chlorosuccinimide, chloramine-T). HBO 2 increased input resistance and stimulated firing rate in 38% of neurons; both effects of HBO 2 were blocked by antioxidant and mimicked by chemical oxidants. Hypercapnia stimulated 32 of 60 (53%) neurons. Remarkably, these CO 2/H ϩ -chemosensitive neurons were preferentially sensitive to HBO2; 90% of neurons sensitive to HBO2 and/or chemical oxidants were also CO2/H ϩ chemosensitive. Conversely, only 19% of HBO2-insensitive neurons were CO2/H ϩ chemosensitive. We conclude that hyperoxia decreases membrane conductance and stimulates firing of putative central CO2/H ϩ -chemoreceptor neurons by an O2 free radical mechanism. These findings may explain why hyperoxia, paradoxically, stimulates ventilation. central chemoreception; reactive oxygen species; cardiorespiratory control; intracellular recording; hyperoxia THE CENTRAL NERVOUS SYSTEM (CNS) is especially sensitive to oxidative stress. For example, hyperoxia, which is a popular model of oxidative stress, induced by breathing high levels of oxygen at hyperbaric pressure [i.e., hyperbaric oxygen (HBO 2 )], can rapidly disrupt neural function and result in CNS O 2 toxicity (16). Neurological responses to hyperoxia vary, depending on the oxygen tension in the brain and the duration of exposure. For example, the CNS response to hyperoxia can range from moderate, but reversible, changes in neural activity (7,49), to violent and reversible seizures at higher levels of oxygen (16), to irreversible motor deficits and ultimately death at the highest dosages of hyperoxia (16). In each of these instances, the effects of hyperoxia on the CNS are thought to result from increased production and accumulation of O 2 free radicals and subsequent oxidation of cellular components vital to maintaining normal mechanisms of neuronal excitability (16).The cardiorespiratory centers of the brain stem, similarly, are sensitive to a broad range of inspired oxygen. Hypoxia increases alveolar ventilation, primarily by stimulation of the peripheral chemoreceptors (18), although a central stimulatory effect on ventilation has also been reported (47, 64). Paradoxica...

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The Effect of Hyperbaric Oxygenation on Retinal Circulation

Frayser¹,

Saltzman²,

Anderson³

et al. 1967

Archives of Ophthalmology

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Oxygen Toxicity. Arterial and Internal Jugular Blood Gas Composition in Man During Inhalation of Air, 100% O₂ and 2% CO₂ in O₂ at 3.5 Atmospheres Ambient Pressure

Cited by 84 publications

References 0 publications

Effects of in vivo hyperoxia on erythrocytes. 3. In vivo peroxidation of erythrocyte lipid.

Effects of in vivo hyperoxia on erythrocytes. 3. In vivo peroxidation of erythrocyte lipid.

Hyperbaric oxygen and chemical oxidants stimulate CO₂/H⁺-sensitive neurons in rat brain stem slices

The Effect of Hyperbaric Oxygenation on Retinal Circulation

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Oxygen Toxicity. Arterial and Internal Jugular Blood Gas Composition in Man During Inhalation of Air, 100% O2 and 2% CO2 in O2 at 3.5 Atmospheres Ambient Pressure

Cited by 84 publications

References 0 publications

Effects of in vivo hyperoxia on erythrocytes. 3. In vivo peroxidation of erythrocyte lipid.

Effects of in vivo hyperoxia on erythrocytes. 3. In vivo peroxidation of erythrocyte lipid.

Hyperbaric oxygen and chemical oxidants stimulate CO2/H+-sensitive neurons in rat brain stem slices

The Effect of Hyperbaric Oxygenation on Retinal Circulation

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Oxygen Toxicity. Arterial and Internal Jugular Blood Gas Composition in Man During Inhalation of Air, 100% O₂ and 2% CO₂ in O₂ at 3.5 Atmospheres Ambient Pressure

Hyperbaric oxygen and chemical oxidants stimulate CO₂/H⁺-sensitive neurons in rat brain stem slices