<i>Oxygen Toxicity. Respiratory Responses of Normal Men to Inhalation of 6 and 100 Per Cent Oxygen Under 3.5 Atmospheres Pressure</i>

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

doi:10.1152/jappl.1953.5.9.487

Cited by 31 publications

(19 citation statements)

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“…This ®nding is in agreement with studies in which CBF was measured using nitrous oxide or 133 xenon methods (Kety and Schmidt 1948;Lambertsen et al 1953;Nakajima et al 1983). Hyperoxia also decreased P ET CO 2 .…”

Section: Discussionsupporting

confidence: 90%

Cerebral blood flow velocity responses to hypoxia in subjects who are susceptible to high-altitude pulmonary oedema

et al. 1999

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Cerebral blood flow increases on exposure to high altitude, and perhaps more so in subjects who develop acute mountain sickness. We determined cerebral blood flow by transcranial Doppler ultrasound of the middle cerebral artery at sea level, in normoxia (fraction of inspired O2, F(I)O2 0.21), and during 15-min periods of either hypoxic (F(I)O2 0.125) or hyperoxic (F(I)O2 1.0) breathing, in 7 subjects with previous high-altitude pulmonary oedema, 6 climbers who had previously tolerated altitudes between 6000 m and 8150 m, and in 20 unselected controls. Hypoxia increased mean middle cerebral artery flow velocity from 69 (3) to 83 (4) cm x s(-1) (P<0.001) in the controls, from 63 (3) to 75 (3) cm x s(-1) (P<0.001) in the high-altitude pulmonary-oedema-susceptible subjects, and from 58 (4) to 70 (4) cm x s(-1) (P<0.001) in the successful high-altitude climbers. Hyperoxia decreased mean middle cerebral flow velocity to 60 (3) cm x s(-1) (P<0.001), 53 (3) cm x s(-1) (P<0.01), and 49 (3) cm x s(-1) (P<0.01) in the controls, high-altitude pulmonary-oedema-susceptible, and high-altitude climbers, respectively. We conclude that a transcranial Doppler-based estimate of cerebral blood flow is affected by hypoxic and hyperoxic breathing, and that it is not predictive of tolerance to high altitude.

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Section: Discussionsupporting

confidence: 90%

Cerebral blood flow velocity responses to hypoxia in subjects who are susceptible to high-altitude pulmonary oedema

et al. 1999

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“…The pHa increased and Pa CO 2 decreased during HBO 2 exposure, a confirmatory finding (22). A previous study reported hypocapnea during hyperbaric oxygen inhalation caused by a central accumulation of CO 2 , contributing to hyperventilation (22).…”

Section: Discussionsupporting

confidence: 59%

“…A previous study reported hypocapnea during hyperbaric oxygen inhalation caused by a central accumulation of CO 2 , contributing to hyperventilation (22).…”

Section: Discussionmentioning

confidence: 95%

“…3) If Pa CO 2 fell sufficiently during HBO 2 exposure, Pv CO 2 might not elevate as expected, since the arterial capillary values were lower. 4) There may be ventilatory effects such as hyperventilation (22) acting independently regarding the reduction seen in Pa CO 2 . 5) It is possible the prior hyperbaric air exposure influenced the CO 2 measurements during subsequent HBO 2 exposure, although we do not have an explanation based on physiological principles.…”

Section: Discussionmentioning

confidence: 99%

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Arterial and pulmonary arterial hemodynamics and oxygen delivery/extraction in normal humans exposed to hyperbaric air and oxygen

Weaver¹,

Howe²,

Snow³

et al. 2009

Journal of Applied Physiology

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Weaver LK, Howe S, Snow GL, Deru K. Arterial and pulmonary arterial hemodynamics and oxygen delivery/extraction in normal humans exposed to hyperbaric air and oxygen. J Appl Physiol 107: 336-345, 2009. First published April 30, 2009 doi:10.1152/japplphysiol.91012.2008.-Divers and hyperbaric chamber attendants breathe hyperbaric air routinely. Hyperbaric oxygen (HBO2) is used therapeutically frequently. Although much is understood about the hemodynamic physiology and gas exchange effects during hyperbaric air and HBO2 exposure, arterial and pulmonary arterial (PA) catheter data, including blood gas values during hyperbaric air and HBO2 exposure of normal humans, have not been reported. We exposed 10 healthy volunteers instrumented with arterial and PA catheters to air at 0.85, 3.0, 2.5, 2.0, 1.3 (decompression stop), 1.12 (decompression stop), and 0.85 atm abs (our altitude) and then at identical pressures breathing O2 followed by atmospheric pressure air while we measured arterial and PA pressures (PAP), cardiac output (Q ), and blood gas measurements from both arterial and PA catheters. Although hemodynamic changes occurred during exposure to both hyperbaric air and HBO2, we observed a greater magnitude of change under HBO2 conditions: heart rate changes ranged from Ϫ9 to Ϫ19% (air to O2), respiratory rate from Ϫ12 to Ϫ17%, Q from Ϫ7 to Ϫ18%, PAP from Ϫ18 to Ϫ19%, pulmonary vascular resistance from Ϫ38 to Ϫ48%, and right-to-left shunt fraction from Ϫ87 to Ϫ107%. Mixed venous CO2 fell 8% from baseline during HBO2 despite mixed venous O2 tensions of several hundred Torr. The stroke volume, O2 delivery, and O2 consumption did not change across exposures. The arterial and mixed venous partial pressures of O2 and contents were elevated, as predicted. O2 extraction increased 37% during HBO2. hyperbaric oxygen; pulmonary arterial catheter; cardiac output; oxygen extraction THOUSANDS OF PATIENTS have been treated with hyperbaric oxygen (HBO 2 ); however, the precise arterial and pulmonary arterial (PA) hemodynamic and gas exchange responses that occur during HBO 2 are not clearly known. Determining precise hemodynamic and gas exchange information requires the subject or patient to be instrumented with arterial and PA (SwanGanz) catheters, permitting measurement of intravascular pressures and blood gases, and PA catheter data collected in normal humans exposed to HBO 2 has been reported only once (24).It has long been established that heart rate (HR) falls during HBO 2 (3). Forty years ago, investigators reported that this reduction in HR was associated with decreased cardiac output (Q ) (48), an observation supported by subsequent research (Table 1) (21,24,27,29,48). Generally accepted hemodynamic effects of HBO 2 now "include mild bradycardia, leading to a proportional decline in Q and a small increase in systemic vascular resistance" (28).As (43), possibly due to high O 2 concentrations reducing myocardial relaxation factor (nitric oxide), thereby making the heart stiffer (23), or by an increase in afterload from i...

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“…One possibility is that high 0 2 causes an increase in C 0 2 in areas adjacent to or bathing the central chemorecep tors. Such C 02 increase would be mediated through cerebral vasoconstriction or reduced ability of hypersaturated hemoglobin to remove C 0 2 from the tissues (6,7). Experimental evidence in animal and human subjects showed that an increase in C 0 2 at the level of the central chemoreceptors is associated with hy perventilation and fast removal of C 0 2 from the cerebrospinal fluid (CSF) (11,12,17).…”

Section: Introductionmentioning

confidence: 99%

Effect of Inhaling 100% O<sub>2</sub> on Ventilation and Acid-Base Balance in Cerebrospinal Fluid of Neonates

Davi¹,

Sankaran²,

Rigatto³

1980

Neonatology

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If 100% O₂ produces hyperventilation by increasing central CO₂ due to cerebral vasoconstriction or diminished reduction of oxyhemoglobin, then, there should be a parallel decrease in alveolar and CSF PCO₂ during O₂ breathing in neonates. To test this hypothesis, we measured ventilation, alveolar PCO₂ and CSF PCO₂, pH and HCO₂ before and 10–20 min after infants began breathing 100% O₂. With 100% O₂, minute ventilation increased from 0.193 ± (SE) 0.013 (n = 7) to 0.252 ± 0.013 liter/min/kg (p < 0.015), P_ACO₂ decreased from 42 ± 2 to 38 ± 2 mm Hg (p < 0.005), CSF PCO₂ decreased from 51 ± 1 to 44 ± 1 mm Hg (p < 0.015), and pH increased from 7.308 ± 0.013 to 7.354 ± 0.013 (p < 0.05). CSF bicarbonate decreased, but not significantly. These findings, showing a trend toward alkalosis, suggest that the neonate, like the adult man, induces hyperventilation during hyperoxia via an increase in PCO₂ at the central level.

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Oxygen Toxicity. Respiratory Responses of Normal Men to Inhalation of 6 and 100 Per Cent Oxygen Under 3.5 Atmospheres Pressure

Cited by 31 publications

References 0 publications

Cerebral blood flow velocity responses to hypoxia in subjects who are susceptible to high-altitude pulmonary oedema

Cerebral blood flow velocity responses to hypoxia in subjects who are susceptible to high-altitude pulmonary oedema

Arterial and pulmonary arterial hemodynamics and oxygen delivery/extraction in normal humans exposed to hyperbaric air and oxygen

Effect of Inhaling 100% O<sub>2</sub> on Ventilation and Acid-Base Balance in Cerebrospinal Fluid of Neonates

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