Perinatal Asphyxia and Brain Development: Mitochondrial Damage Without Anatomical or Cellular Losses

Lima, Jean Pierre Mendes; Rayêe, Danielle; Silva-Rodrigues, Thaia; Pereira, Patrı́cia; Mendonça, Ana Paula M.; Rodrigues-Ferreira, Clara; Szczupak, Diego; Fonseca, Adelaida Pallavicini; Oliveira, Moacir Franco de; Lima, Flávia Regina Souza; Lent, Roberto; Galina, Antônio; Uziel, Daniela

doi:10.1016/j.bbabio.2018.09.224

Biochimica et Biophysica Acta (BBA) - Bioenergetics

2018

DOI: 10.1016/j.bbabio.2018.09.224

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Perinatal Asphyxia and Brain Development: Mitochondrial Damage Without Anatomical or Cellular Losses

Jean Pierre Mendes Lima

Danielle Rayêe

Thaia Silva-Rodrigues

et al.

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“…As oxygenation is restored and aerobic respiration resumes, the kinetics of brain oxygen consumption is not known. We considered that brain oxygen consumption may rise in response to the accumulated oxygen deficit in keeping with mitochondrial studies of mild-moderate perinatal asphyxia 11,12 , or remain depressed from the antecedent asphyxia and ongoing suppression of cellular metabolic activity. Excessive oxygen exposure to the asphyxic neonatal brain is associated with free-radical mediated injury and apoptosis 13 .…”

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Excess cerebral oxygen delivery follows return of spontaneous circulation in near-term asphyxiated lambs

Badurdeen

Gill

Kluckow

et al. 2020

Sci Rep

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Hypoxic-ischaemia renders the neonatal brain susceptible to early secondary injury from oxidative stress and impaired autoregulation. We aimed to describe cerebral oxygen kinetics and haemodynamics immediately following return of spontaneous circulation (ROSC) and evaluate non-invasive parameters to facilitate bedside monitoring. Near-term sheep fetuses [139 ± 2 (SD) days gestation, n = 16] were instrumented to measure carotid artery (CA) flow, pressure, right brachial arterial and jugular venous saturation (SaO2 and SvO2, respectively). Cerebral oxygenation (crSO2) was measured using near-infrared spectroscopy (NIRS). Following induction of severe asphyxia, lambs received cardiopulmonary resuscitation using 100% oxygen until ROSC, with oxygen subsequently weaned according to saturation nomograms as per current guidelines. We found that oxygen consumption did not rise following ROSC, but oxygen delivery was markedly elevated until 15 min after ROSC. CrSO2 and heart rate each correlated with oxygen delivery. SaO2 remained > 90% and was less useful for identifying trends in oxygen delivery. CrSO2 correlated inversely with cerebral fractional oxygen extraction. In conclusion, ROSC from perinatal asphyxia is characterised by excess oxygen delivery that is driven by rapid increases in cerebrovascular pressure, flow, and oxygen saturation, and may be monitored non-invasively. Further work to describe and limit injury mediated by oxygen toxicity following ROSC is warranted.

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confidence: 99%

Excess cerebral oxygen delivery follows return of spontaneous circulation in near-term asphyxiated lambs

Badurdeen

Gill

Kluckow

et al. 2020

Sci Rep

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Risk factors for asphyxia neonatorum in public health centres of nosarara and pantoloan, Palu City

Fitriana

Mallongi

et al. 2021

Gaceta Sanitaria

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Perinatal Asphyxia and Brain Development: Mitochondrial Damage Without Anatomical or Cellular Losses

Cited by 2 publications

References 0 publications

Excess cerebral oxygen delivery follows return of spontaneous circulation in near-term asphyxiated lambs

Excess cerebral oxygen delivery follows return of spontaneous circulation in near-term asphyxiated lambs

Risk factors for asphyxia neonatorum in public health centres of nosarara and pantoloan, Palu City

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