Brain alkalosis causes birth asphyxia seizures, suggesting therapeutic strategy

Helmy, Mohamed M.; Tolner, Else A.; Vanhatalo, Sampsa; Voipio, Juha; Kaila, Kai

doi:10.1002/ana.22223

Cited by 52 publications

(83 citation statements)

References 40 publications

(91 reference statements)

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“…The pronounced suppression of GDPs by a very small acid load (as seen with 1 mM propionate) indicates that neonatal neurons are exquisitely sensitive to changes in pH i . This finding is likely to have important implications on the generation of endogenous network events under physiological and pathophysiological conditions (Helmy et al, 2010) in the developing brain.…”

Section: Discussionmentioning

confidence: 83%

Spontaneous Network Events Driven by Depolarizing GABA Action in Neonatal Hippocampal Slices are Not Attributable to Deficient Mitochondrial Energy Metabolism

Ruusuvuori

Kirilkin

Pandya³

et al. 2010

J. Neurosci.

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Section: Discussionmentioning

confidence: 83%

Spontaneous Network Events Driven by Depolarizing GABA Action in Neonatal Hippocampal Slices are Not Attributable to Deficient Mitochondrial Energy Metabolism

Ruusuvuori

Kirilkin

Pandya³

et al. 2010

J. Neurosci.

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“…A recent study by Zhou et al (25) showed in an animal model that moderate hypercapnia may be protective following global cerebral ischemia. In addition, brain alkalosis has been shown to induce seizure activity in rodents after asphyxia (26). Ventilation strategies are of great relevance since a previous Finnish study showed a high prevalence of hypocapnia in patients treated with TH (27).…”

Section: Discussionmentioning

confidence: 99%

Arterial Blood Gas Tensions After Resuscitation From Out-of-Hospital Cardiac Arrest

Vaahersalo

Bendel

Reinikainen

et al. 2014

Critical Care Medicine

154

119

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“…To mimic a persistent impaired gas exchange leading to hypoxia and hypercapnia, as seen during asphyxia, P6 pups of both genders randomly separated from 5 mothers from each dietary group (n = 28 pups/group) were exposed to a gas mixture of 9% O 2 and 20% CO 2 in N 2 for 90 min, as previously described [11], using a birth asphyxia model developed by Helmy et al [12]. All pups survived the exposure and were immediately returned to their mothers for 24-48 h. Two experimental groups resulted: PA group (PA-exposed pups whose mothers received standard diet) and HF-PA group (PA-exposed pups whose mothers received HFD).…”

Section: Animals and Experimental Conditionsmentioning

confidence: 99%

Maternal High-Fat Diet Modifies the Immature Hippocampus Vulnerability to Perinatal Asphyxia in Rats

Isac¹,

Panaitescu²,

Ieșanu

et al. 2018

Neonatology

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Background: High-fat diet (HFD) is a detrimental habit with harmful systemic consequences, including low-grade, long-lasting inflammation. During pregnancy, HFD can induce developmental changes. Moreover, HFD-related maternal obesity might enhance the risk of peripartum complications including hypoxic-ischemic encephalopathy secondary to perinatal asphyxia (PA). Objectives: Following our previous results showing that PA increases neuroinflammation and neuronal injury in the immature hippocampus and modifies hippocampal epigenetic programming, we further aimed to establish the impact of maternal HFD on offspring hippocampus response to PA. Methods: We assessed hippocampal tumor necrosis factor alpha (TNFα), interleukin 1 beta (IL-1b) and S-100B protein (S-100B), 24–48 h after PA exposure in postnatal day 6 Wistar rats, whose mothers received either the standard diet or HFD. The expression of small non-coding microRNA species miR124, miR132, miR134, miR146, and miR15a, as epigenetic markers for the maternal dietary influence on immature hippocampus response after PA, was determined 24 h after asphyxia exposure. Metabolic activity was measured using resazurin test in hippocampal cell suspension obtained 24 h after PA. Results: Our results indicate that maternal HFD additionally increases hippocampal TNFα, IL-1b, and S-100B after PA. Also, PA associated with maternal HFD induces miR124 upregulation and miR132 downregulation relative to PA only. Metabolic activity was increased in hippocampal cells from pups whose mothers received HFD. Conclusion: HFD increases the PA-induced neuroinflammation and neuronal injury, and epigenetically influences homeostatic synaptic plasticity and neuronal tolerance to asphyxia, processes associated with a higher hippocampal cellular metabolism.

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Brain alkalosis causes birth asphyxia seizures, suggesting therapeutic strategy

Cited by 52 publications

References 40 publications

Spontaneous Network Events Driven by Depolarizing GABA Action in Neonatal Hippocampal Slices are Not Attributable to Deficient Mitochondrial Energy Metabolism

Spontaneous Network Events Driven by Depolarizing GABA Action in Neonatal Hippocampal Slices are Not Attributable to Deficient Mitochondrial Energy Metabolism

Arterial Blood Gas Tensions After Resuscitation From Out-of-Hospital Cardiac Arrest

Maternal High-Fat Diet Modifies the Immature Hippocampus Vulnerability to Perinatal Asphyxia in Rats

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