Surge of Peripheral Arginine Vasopressin in a Rat Model of Birth Asphyxia

Show simple item record Summanen, Milla Back, Susanne Voipio, Juha Kaila, Kai 2018-03-15T09:11:01Z 2018-03-15T09:11:01Z 2018-01-19
dc.identifier.citation Summanen , M , Back , S , Voipio , J & Kaila , K 2018 , ' Surge of Peripheral Arginine Vasopressin in a Rat Model of Birth Asphyxia ' , Frontiers in Cellular Neuroscience , vol. 12 , 2 .
dc.identifier.other PURE: 100384592
dc.identifier.other PURE UUID: 769a0960-17ac-4850-b770-c623e3779510
dc.identifier.other WOS: 000423000200001
dc.identifier.other Scopus: 85041468812
dc.identifier.other ORCID: /0000-0003-3843-2741/work/42819840
dc.identifier.other ORCID: /0000-0003-0668-5955/work/42819236
dc.identifier.other ORCID: /0000-0001-7096-1286/work/42819386
dc.description.abstract Mammalian birth is accompanied by a period of obligatory asphyxia, which consists of hypoxia (drop in blood O-2 levels) and hypercapnia (elevation of blood CO2 levels). Prolonged, complicated birth can extend the asphyxic period, leading to a pathophysiological situation, and in humans, to the diagnosis of clinical birth asphyxia, the main cause of hypoxic-ischemic encephalopathy (HIE). The neuroendocrine component of birth asphyxia, in particular the increase in circulating levels of arginine vasopressin (AVP), has been extensively studied in humans. Here we show for the first time that normal rat birth is also accompanied by an AVP surge, and that the fetal AVP surge is further enhanced in a model of birth asphyxia, based on exposing 6-day old rat pups to a gas mixture containing 4% O-2 and 20% CO2 for 45 min. Instead of AVP, which is highly unstable with a short plasma half-life, we measured the levels of copeptin, the C-terminal part of prepro-AVP that is biochemically much more stable. In our animal model, the bulk of AVP/copeptin release occurred at the beginning of asphyxia (mean 7.8 nM after 15 min of asphyxia), but some release was still ongoing even 90 min after the end of the 45 min experimental asphyxia (mean 1.2 nM). Notably, the highest copeptin levels were measured after hypoxia alone (mean 14.1 nM at 45 min), whereas copeptin levels were low during hypercapnia alone (mean 2.7 nM at 45 min), indicating that the hypoxia component of asphyxia is responsible for the increase in AVP/copeptin release. Alternating the O-2 level between 5 and 9% (CO2 at 20%) with 5 min intervals to mimic intermittent asphyxia during prolonged labor resulted in a slower but quantitatively similar rise in copeptin (peak of 8.3 nM at 30 min). Finally, we demonstrate that our rat model satisfies the standard acid-base criteria for birth asphyxia diagnosis, namely a drop in blood pH below 7.0 and the formation of a negative base excess exceeding -11.2 mmol/l. The mechanistic insights from our work validate the use of the present rodent model in preclinical work on birth asphyxia. en
dc.format.extent 9
dc.language.iso eng
dc.relation.ispartof Frontiers in Cellular Neuroscience
dc.rights cc_by
dc.rights.uri info:eu-repo/semantics/openAccess
dc.subject arginine vasopressin (AVP)
dc.subject copeptin
dc.subject birth asphyxia
dc.subject hypothalamic-pituitary axis (HPA axis)
dc.subject blood gases
dc.subject base deficit
dc.subject perinatal
dc.subject neonatal
dc.subject COPEPTIN
dc.subject BRAIN
dc.subject HYPOXIA
dc.subject STRESS
dc.subject PRECURSOR
dc.subject RELEASE
dc.subject NEURONS
dc.subject 3112 Neurosciences
dc.subject 3124 Neurology and psychiatry
dc.title Surge of Peripheral Arginine Vasopressin in a Rat Model of Birth Asphyxia en
dc.type Article
dc.contributor.organization Biosciences
dc.contributor.organization Laboratory of Neurobiology
dc.contributor.organization Juha Voipio / Principal Investigator
dc.contributor.organization Physiology and Neuroscience (-2020)
dc.contributor.organization Kai Kaila / Principal Investigator
dc.contributor.organization Neuroscience Center
dc.description.reviewstatus Peer reviewed
dc.relation.issn 1662-5102
dc.rights.accesslevel openAccess
dc.type.version publishedVersion

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