Systemic inflammation exacerbates developmental neurotoxicity induced by sevoflurane in neonatal rats.


Journal

British journal of anaesthesia
ISSN: 1471-6771
Titre abrégé: Br J Anaesth
Pays: England
ID NLM: 0372541

Informations de publication

Date de publication:
10 2022
Historique:
received: 21 09 2021
revised: 14 04 2022
accepted: 08 05 2022
pubmed: 15 6 2022
medline: 6 10 2022
entrez: 14 6 2022
Statut: ppublish

Résumé

General anaesthesia in the neonatal period has detrimental effects on the developing mammalian brain. The impact of underlying inflammation on anaesthesia-induced developmental neurotoxicity remains largely unknown. Postnatal day 7 (PND7) rats were randomly assigned to receive sevoflurane (3 vol% for 3 h) or carrier gas 12 h after bacterial lipopolysaccharide (LPS; 1 μg g Sevoflurane or LPS treatment increased activated caspase-3 and caspase-9 expression in the hippocampal subiculum and CA1, which was greater when sevoflurane was administered in the setting of LPS-induced inflammation. Neuronal injury induced by LPS+sevoflurane treatment resulted in sex-specific behavioural outcomes when rats were tested at 5-8 weeks of age, including learning and memory deficits in males and heightened anxiety-related behaviour in females. Hippocampal caspase-1 and NLRP1 (NLR family pyrin domain containing 1), but not NLRP3, were upregulated by LPS or LPS+sevoflurane treatment, along with related proinflammatory cytokines, interleukin (IL)-1β, and IL-18. Pretreatment with Vx-765, a selective caspase-1 inhibitor, led to reduced IL-1β in LPS and LPS+sevoflurane groups. Caspase-1 inhibition by Vx-765 significantly decreased activated caspase-3 and caspase-9 immunoreactivity in the subiculum. Systemic inflammation promotes developmental neurotoxicity by worsening anaesthesia-induced neuronal damage with sex-specific behavioural outcomes. This highlights the importance of studying anaesthesia-induced neurotoxicity in more clinically relevant settings.

Sections du résumé

BACKGROUND
General anaesthesia in the neonatal period has detrimental effects on the developing mammalian brain. The impact of underlying inflammation on anaesthesia-induced developmental neurotoxicity remains largely unknown.
METHODS
Postnatal day 7 (PND7) rats were randomly assigned to receive sevoflurane (3 vol% for 3 h) or carrier gas 12 h after bacterial lipopolysaccharide (LPS; 1 μg g
RESULTS
Sevoflurane or LPS treatment increased activated caspase-3 and caspase-9 expression in the hippocampal subiculum and CA1, which was greater when sevoflurane was administered in the setting of LPS-induced inflammation. Neuronal injury induced by LPS+sevoflurane treatment resulted in sex-specific behavioural outcomes when rats were tested at 5-8 weeks of age, including learning and memory deficits in males and heightened anxiety-related behaviour in females. Hippocampal caspase-1 and NLRP1 (NLR family pyrin domain containing 1), but not NLRP3, were upregulated by LPS or LPS+sevoflurane treatment, along with related proinflammatory cytokines, interleukin (IL)-1β, and IL-18. Pretreatment with Vx-765, a selective caspase-1 inhibitor, led to reduced IL-1β in LPS and LPS+sevoflurane groups. Caspase-1 inhibition by Vx-765 significantly decreased activated caspase-3 and caspase-9 immunoreactivity in the subiculum.
CONCLUSIONS
Systemic inflammation promotes developmental neurotoxicity by worsening anaesthesia-induced neuronal damage with sex-specific behavioural outcomes. This highlights the importance of studying anaesthesia-induced neurotoxicity in more clinically relevant settings.

Identifiants

pubmed: 35701270
pii: S0007-0912(22)00246-X
doi: 10.1016/j.bja.2022.05.008
pmc: PMC10080473
pii:
doi:

Substances chimiques

Cytokines 0
Interleukin-18 0
Lipopolysaccharides 0
Sevoflurane 38LVP0K73A
Caspase 3 EC 3.4.22.-
Caspase 9 EC 3.4.22.-
Caspase 1 EC 3.4.22.36

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

555-566

Subventions

Organisme : NICHD NIH HHS
ID : R01 HD097990
Pays : United States

Informations de copyright

Copyright © 2022 British Journal of Anaesthesia. Published by Elsevier Ltd. All rights reserved.

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Auteurs

Nemanja Useinovic (N)

Department of Anesthesiology, University of Colorado Anschutz Medical Campus, Aurora, CO, USA. Electronic address: nemanja.useinovic@cuanschutz.edu.

Stefan Maksimovic (S)

Department of Anesthesiology, University of Colorado Anschutz Medical Campus, Aurora, CO, USA.

Cole Liechty (C)

Department of Anesthesiology, University of Colorado Anschutz Medical Campus, Aurora, CO, USA.

Omar H Cabrera (OH)

Department of Anesthesiology, University of Colorado Anschutz Medical Campus, Aurora, CO, USA.

Nidia Quillinan (N)

Department of Anesthesiology, University of Colorado Anschutz Medical Campus, Aurora, CO, USA; Neuronal Injury and Plasticity Program, University of Colorado Anschutz Medical Campus, Aurora, CO, USA.

Vesna Jevtovic-Todorovic (V)

Department of Anesthesiology, University of Colorado Anschutz Medical Campus, Aurora, CO, USA; Department of Pharmacology, University of Colorado Anschutz Medical Campus, Aurora, CO, USA.

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Classifications MeSH