Hypercapnia Causes Injury of the Cerebral Cortex and Cognitive Deficits in Newborn Piglets


Journal article


Karen Fritz, Georgios Sanidas, Rodolfo Cardenas, Javid Ghaemmaghami, Chad Byrd, Gabriele Simonti, Adriana Valenzuela, Ignacio Valencia, Maria Delivoria-Papadopoulos, Vittorio Gallo, Ioannis Koutroulis, Terry Dean, Panagiotis Kratimenos
eNeuro, 2024

Semantic Scholar DOI PubMedCentral PubMed
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APA   Click to copy
Fritz, K., Sanidas, G., Cardenas, R., Ghaemmaghami, J., Byrd, C., Simonti, G., … Kratimenos, P. (2024). Hypercapnia Causes Injury of the Cerebral Cortex and Cognitive Deficits in Newborn Piglets. ENeuro.


Chicago/Turabian   Click to copy
Fritz, Karen, Georgios Sanidas, Rodolfo Cardenas, Javid Ghaemmaghami, Chad Byrd, Gabriele Simonti, Adriana Valenzuela, et al. “Hypercapnia Causes Injury of the Cerebral Cortex and Cognitive Deficits in Newborn Piglets.” eNeuro (2024).


MLA   Click to copy
Fritz, Karen, et al. “Hypercapnia Causes Injury of the Cerebral Cortex and Cognitive Deficits in Newborn Piglets.” ENeuro, 2024.


BibTeX   Click to copy

@article{karen2024a,
  title = {Hypercapnia Causes Injury of the Cerebral Cortex and Cognitive Deficits in Newborn Piglets},
  year = {2024},
  journal = {eNeuro},
  author = {Fritz, Karen and Sanidas, Georgios and Cardenas, Rodolfo and Ghaemmaghami, Javid and Byrd, Chad and Simonti, Gabriele and Valenzuela, Adriana and Valencia, Ignacio and Delivoria-Papadopoulos, Maria and Gallo, Vittorio and Koutroulis, Ioannis and Dean, Terry and Kratimenos, Panagiotis}
}

Abstract

In critically ill newborns, exposure to hypercapnia (HC) is common and often accepted in neonatal intensive care units to prevent severe lung injury. However, as a “safe” range of arterial partial pressure of carbon dioxide levels in neonates has not been established, the potential impact of HC on the neurodevelopmental outcomes in these newborns remains a matter of concern. Here, in a newborn Yorkshire piglet model of either sex, we show that acute exposure to HC induced persistent cortical neuronal injury, associated cognitive and learning deficits, and long-term suppression of cortical electroencephalogram frequencies. HC induced a transient energy failure in cortical neurons, a persistent dysregulation of calcium-dependent proapoptotic signaling in the cerebral cortex, and activation of the apoptotic cascade, leading to nuclear deoxyribonucleic acid fragmentation. While neither 1 h of HC nor the rapid normalization of HC was associated with changes in cortical bioenergetics, rapid resuscitation resulted in a delayed onset of synaptosomal membrane lipid peroxidation, suggesting a dissociation between energy failure and the occurrence of synaptosomal lipid peroxidation. Even short durations of HC triggered biochemical responses at the subcellular level of the cortical neurons resulting in altered cortical activity and impaired neurobehavior. The deleterious effects of HC on the developing brain should be carefully considered as crucial elements of clinical decisions in the neonatal intensive care unit.


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