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

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http://hdl.handle.net/10138/317402

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Pospelov , A S , Puskarjov , M , Kaila , K & Voipio , J 2020 , ' Endogenous brain-sparing responses in brain pH and PO2 in a rodent model of birth asphyxia ' , Acta Physiologica , vol. 229 , no. 3 , 13467 . https://doi.org/10.1111/apha.13467

Title: Endogenous brain-sparing responses in brain pH and PO2 in a rodent model of birth asphyxia
Author: Pospelov, Alexey S.; Puskarjov, Martin; Kaila, Kai; Voipio, Juha
Contributor: University of Helsinki, Molecular and Integrative Biosciences Research Programme
University of Helsinki, Molecular and Integrative Biosciences Research Programme
University of Helsinki, Molecular and Integrative Biosciences Research Programme
University of Helsinki, Molecular and Integrative Biosciences Research Programme
Date: 2020-07
Language: eng
Number of pages: 18
Belongs to series: Acta Physiologica
ISSN: 1748-1708
URI: http://hdl.handle.net/10138/317402
Abstract: Abstract 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 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.
Subject: 3112 Neurosciences
brain pH and oxygen
brain protection
graded restoration of normocapnia
HIE
perinatal asphyxia
physiology
TISSUE OXYGENATION
PROTON MODULATION
PERIVENTRICULAR LEUKOMALACIA
GUINEA-PIG
PERINATAL ASPHYXIA
PERMISSIVE HYPERCAPNIA
ANIMAL-MODEL
GABA(A) RECEPTORS
CARBON-DIOXIDE
NEWBORN-INFANTS
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