The oxyhemoglobin dissociation curve in hypercapnic patients

Agostoni, A; Stabilint, R.; Bernasconi, C.; Gerli, Giancarla

doi:10.1016/0002-8703(74)90509-2

Cited by 5 publications

(3 citation statements)

References 8 publications

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“…While studies monitoring CBF have shed light on adaptive responses acting to maintain brain oxygenation, it is obvious that CBF data do not provide direct information on the level oxygen in brain tissue during asphyxia. For instance, during asphyxia, CBF increases but at the same time there is not only a large decline in O 2 availability but also a large fall in blood pH, which reduces the oxygen carrying capacity of blood because of the Bohr effect 75‐77 . Thus, measurements of PO 2 in brain tissue provide direct quantitative information on this key variable, as is the case in the present study.…”

Section: Discussionsupporting

confidence: 55%

“…For instance, during asphyxia, CBF increases but at the same time there is not only a large decline in O 2 availability but also a large fall in blood pH, which reduces the oxygen carrying capacity of blood because of the Bohr effect. [75][76][77] Thus, measurements of PO 2 in brain tissue provide direct quantitative information on this key variable, as is the case in the present study. A direct demonstration of the CO 2 -dependence of brain oxygenation during asphyxia is that while hypoxia brought about by lowering ambient O 2 to 9% causes a near-instantaneous fall in brain PO 2 to about one tenth of the baseline level, nearly normoxic conditions prevail in the brain parenchyma when the same level of hypoxia is combined with hypercapnia.…”

Section: Brain-protecting Systemslevel Mechanismssupporting

confidence: 56%

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Endogenous brain‐sparing responses in brain pH and PO₂ in a rodent model of birth asphyxia

et al. 2020

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Aim To study brain‐sparing physiological responses in a rodent model of birth asphyxia which reproduces the asphyxia‐defining systemic hypoxia and hypercapnia. Methods Steady or intermittent asphyxia was induced for 15‐45 minutes in anaesthetized 6‐ and 11‐days old rats and neonatal guinea pigs using gases containing 5% or 9% O2 plus 20% CO2 (in N2). Hypoxia and hypercapnia were induced with low O2 and high CO2 respectively. Oxygen partial pressure (PO2) and pH were measured with microsensors within the brain and subcutaneous (“body”) tissue. Blood lactate was measured after asphyxia. Results Brain and body PO2 fell to apparent zero with little recovery during 5% O2 asphyxia and 5% or 9% O2 hypoxia, and increased more than twofold during 20% CO2 hypercapnia. Unlike body PO2, brain PO2 recovered rapidly to control after a transient fall (rat), or was slightly higher than control (guinea pig) during 9% O2 asphyxia. Asphyxia (5% O2) induced a respiratory acidosis paralleled by a progressive metabolic (lact)acidosis that was much smaller within than outside the brain. Hypoxia (5% O2) produced a brain‐confined alkalosis. Hypercapnia outlasting asphyxia suppressed pH recovery and prolonged the post‐asphyxia PO2 overshoot. All pH changes were accompanied by consistent shifts in the blood‐brain barrier potential. Conclusion Regardless of brain maturation stage, hypercapnia can restore brain PO2 and protect the brain against metabolic acidosis despite compromised oxygen availability during asphyxia. This effect extends to the recovery phase if normocapnia is restored slowly, and it is absent during hypoxia, demonstrating that exposure to hypoxia does not mimic asphyxia.

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Section: Discussionsupporting

confidence: 55%

Section: Brain-protecting Systemslevel Mechanismssupporting

confidence: 56%

Endogenous brain‐sparing responses in brain pH and PO₂ in a rodent model of birth asphyxia

et al. 2020

View full text Add to dashboard Cite

show abstract

“…For instance, during asphyxia, CBF increases but at the same time there is not only a large decline in O2 availability but also a large fall in blood pH, which reduces the oxygen carrying capacity of blood because of the Bohr effect. [75][76][77] Thus, measurements of P O 2 in brain tissue provide direct quantitative information on this key variable, as is the case in the present study. A direct demonstration of the CO2-dependence of brain oxygenation during asphyxia is that while hypoxia brought about by lowering ambient O2 to 9% causes a near-instantaneous fall in brain P O 2 to about one tenth of the baseline level, nearly normoxic conditions prevail in the brain parenchyma when the same level of hypoxia is combined with hypercapnia.…”

Section: Brain-protecting Systems-level Mechanismssupporting

confidence: 57%

Endogenous responses in brain pH andP_O2in a rodent model of birth asphyxia

Puskarjov

Kaila

et al. 2019

Preprint

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Aim:To study brain-sparing physiological responses in a rodent model of birth asphyxia which reproduces the asphyxia-defining systemic hypoxia and hypercapnia.Methods: Steady or intermittent asphyxia was induced for 15-45 min in anesthetized 6 and 11 days old rats and neonatal guinea pigs using gases containing 5% or 9% O2 plus 20% CO2 (in N2).Hypoxia and hypercapnia were induced with low O2 and high CO2, respectively. Oxygen partial pressure (PO2) and pH were measured with microsensors within the brain and subcutaneous ("body") tissue. Blood lactate was measured after asphyxia.Results: Brain and body PO2 fell to apparent zero with little recovery during 5% O2 asphyxia and 5% or 9% O2 hypoxia, and increased more than twofold during 20% CO2 hypercapnia. Unlike body PO2, brain PO2 recovered rapidly to control after a transient fall (rat), or was slightly higher than control (guinea pig) during 9% O2 asphyxia. Asphyxia (5% O2) induced a respiratory acidosis paralleled by a progressive metabolic (lact)acidosis that was much smaller within than outside the brain. Hypoxia (5% O2) produced brain-confined alkalosis. Hypercapnia outlasting asphyxia suppressed pH recovery and prolonged the post-asphyxia PO2 overshoot. All pH changes were accompanied by consistent shifts in the blood-brain barrier potential. Conclusion:Regardless of brain maturation stage, hypercapnia can restore brain PO2 and protect the brain against metabolic acidosis despite compromised oxygen availability during asphyxia. This effect extends to recovery phase if normocapnia is restored slowly, and it is absent during hypoxia, demonstrating that exposure to hypoxia does not mimic asphyxia.

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Hemoglobin oxygen affinity in patients with acute myocardial infarction and angina pectoris

Agostoni

1976

Physiological and Clinical Aspects of Oxygenator Design

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The oxyhemoglobin dissociation curve in hypercapnic patients

Cited by 5 publications

References 8 publications

Endogenous brain‐sparing responses in brain pH and PO₂ in a rodent model of birth asphyxia

Endogenous brain‐sparing responses in brain pH and PO₂ in a rodent model of birth asphyxia

Endogenous responses in brain pH andP_O2in a rodent model of birth asphyxia

Hemoglobin oxygen affinity in patients with acute myocardial infarction and angina pectoris

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The oxyhemoglobin dissociation curve in hypercapnic patients

Cited by 5 publications

References 8 publications

Endogenous brain‐sparing responses in brain pH and PO2 in a rodent model of birth asphyxia

Endogenous brain‐sparing responses in brain pH and PO2 in a rodent model of birth asphyxia

Endogenous responses in brain pH andPO2in a rodent model of birth asphyxia

Hemoglobin oxygen affinity in patients with acute myocardial infarction and angina pectoris

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Product

Resources

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Endogenous brain‐sparing responses in brain pH and PO₂ in a rodent model of birth asphyxia

Endogenous brain‐sparing responses in brain pH and PO₂ in a rodent model of birth asphyxia

Endogenous responses in brain pH andP_O2in a rodent model of birth asphyxia