Newborn Transition to Extrauterine Life

Vanwoudenberg, Christine D.; Wills, C.; Rubarth, Lori Baas

doi:10.1891/0730-0832.31.5.317

Cited by 11 publications

(11 citation statements)

References 6 publications

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“…By definition, asphyxia implies a fall in blood O 2 (hypoxia) that is associated with an elevation of CO 2 (hypercapnia). This period of obligatory, non-pathophysiological asphyxia is an essential part of the “stress of birth” (Van Woudenberg et al, 2012 ; Evers and Wellman, 2016 ), which is beneficial in that it activates the hypothalamic-pituitary axis (the HPA axis) as well as the sympathetic nervous system. This, in turn, triggers a wide range of cardiovascular and pulmonary responses facilitating the adaptation of the newborn individual to extra-uterine life (Lagercrantz and Slotkin, 1986 ; Van Woudenberg et al, 2012 ; Lagercrantz, 2016 ).…”

Section: Introductionmentioning

confidence: 99%

“…This period of obligatory, non-pathophysiological asphyxia is an essential part of the “stress of birth” (Van Woudenberg et al, 2012 ; Evers and Wellman, 2016 ), which is beneficial in that it activates the hypothalamic-pituitary axis (the HPA axis) as well as the sympathetic nervous system. This, in turn, triggers a wide range of cardiovascular and pulmonary responses facilitating the adaptation of the newborn individual to extra-uterine life (Lagercrantz and Slotkin, 1986 ; Van Woudenberg et al, 2012 ; Lagercrantz, 2016 ). However, a prolonged period of birth asphyxia is harmful, causing dysfunction and damage with lifelong consequences in organ systems with a high and predominantly aerobic energy metabolism, such as the brain (Painter, 1995 ; Fattuoni et al, 2015 ; Ahearne et al, 2016 ).…”

Section: Introductionmentioning

confidence: 99%

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

Summanen

Bäck

Voipio

et al. 2018

Front. Cell. Neurosci.

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Mammalian birth is accompanied by a period of obligatory asphyxia, which consists of hypoxia (drop in blood O2 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% O2 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 O2 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.

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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

Summanen

Bäck

Voipio

et al. 2018

Front. Cell. Neurosci.

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“…Among these responses are the regulation of cardiac function via stimulation of α-adrenergic receptors (prior to the subsequent switch over to the adult β-adrenergic receptors), and initiation of lung respiration (Slotkin and Seidler, 1988). The latter involves the stimulation of surfactant secretion via β 2 -receptors, and transformation of the physiological properties of the lung epithelium from a state where fluid is secreted to one where fluid is reabsorbed (Olver et al, 1986;Van Woudenberg et al, 2012). In the developing rat embryo, the release of CAT during hypoxic stress has been proposed to promote fetal survival by reversing hypoxia-induced bradycardia, thereby maintaining O 2 homeostasis (Ream et al, 2008).…”

Section: Introductionmentioning

confidence: 99%

Ontogeny of O2 and CO2//H+ chemosensitivity in adrenal chromaffin cells: role of innervation

Salman

Buttigieg

Nurse

2014

Journal of Experimental Biology

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The adrenal medulla plays a key role in the physiological responses of developing and mature mammals by releasing catecholamines (CAT) during stress. In rodents and humans, the innervation of CATproducing, adrenomedullary chromaffin cells (AMCs) is immature or absent during early postnatal life, when these cells possess 'direct' hypoxia-and CO 2 /H + -chemosensing mechanisms. During asphyxial stressors at birth, these mechanisms contribute to a CAT surge that is critical for adaptation to extra-uterine life. These direct chemosensing mechanisms regress postnatally, in parallel with maturation of splanchnic innervation. Here, we review the evidence that neurotransmitters released from the splanchnic nerve during innervation activate signaling cascades that ultimately cause regression of direct AMC chemosensitivity to hypoxia and hypercapnia. In particular, we consider the roles of cholinergic and opioid receptor signaling, given that splanchnic nerves release acetylcholine and opiate peptides onto their respective postsynaptic nicotinic and opioid receptors on AMCs. Recent in vivo and in vitro studies in the rat suggest that interactions involving α7 nicotinic acetylcholine receptors (nAChRs), the hypoxia inducible factor (HIF)-2α signaling pathway, protein kinases and ATP-sensitive K + (K ATP ) channels contribute to the selective suppression of hypoxic chemosensitivity. In contrast, interactions involving μ-and/or δ-opiod receptor signaling pathways contribute to the suppression of both hypoxic and hypercapnic chemosensitivity, via regulation of the expression of K ATP channels and carbonic anhydrase (CA I and II), respectively. These data suggest that the ontogeny of O 2 and CO 2 /H + chemosensitivity in chromaffin cells can be regulated by the tonic release of presynaptic neurotransmitters.

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“…Within 12 to 24 hours the newborn diureses, mobilizing extracellular fluid and decreasing that compartment from 40% at birth to 30%. This fluid loss accounts for much of the weight loss that occurs over the first 5 days …”

Section: Further Adaptations To Extrauterine Lifementioning

confidence: 99%

Newborn Transition

Graves¹,

Haley²

2013

J Midwife Womens Health

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The transition from intrauterine to extrauterine life is a complex adaptation. Although, in a sense, the entire time in utero is in preparation for this transition, there are many specific anatomic and physiologic changes that take place in the weeks and days leading up to labor that facilitate a healthy transition. Some, including increasing pulmonary vasculature and blood flow, are part of an ongoing process of maturation. Others, such as a reversal in the lung from secreting fluid to absorbing fluid and the secretion of pulmonary surfactant, are associated with the hormonal milieu that occurs when spontaneous labor is impending. Interventions such as elective cesarean birth or induction of labor may interfere with this preparation for birth. Postnatal interventions such as immediate clamping of the umbilical cord and oropharyngeal suction may also compromise the normal process of newborn transition. This article reviews the physiology of the fetal to newborn transition and explores interventions that may facilitate or hinder the optimal process.

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Newborn Transition to Extrauterine Life

Cited by 11 publications

References 6 publications

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

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

Ontogeny of O2 and CO2//H+ chemosensitivity in adrenal chromaffin cells: role of innervation

Newborn Transition

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