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The O(2)-sensitive brain stem, hyperoxic hyperventilation, and CNS oxygen toxicity

Central nervous system oxygen toxicity (CNS-OT) is a complex disorder that presents, initially, as a sequence of cardio-respiratory abnormalities and nonconvulsive signs and symptoms (S/Sx) of brain stem origin that culminate in generalized seizures, loss of consciousness, and postictal cardiogenic...

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Autores principales: Dean, Jay B., Stavitzski, Nicole M.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Frontiers Media S.A. 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9360621/
https://www.ncbi.nlm.nih.gov/pubmed/35957982
http://dx.doi.org/10.3389/fphys.2022.921470
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author Dean, Jay B.
Stavitzski, Nicole M.
author_facet Dean, Jay B.
Stavitzski, Nicole M.
author_sort Dean, Jay B.
collection PubMed
description Central nervous system oxygen toxicity (CNS-OT) is a complex disorder that presents, initially, as a sequence of cardio-respiratory abnormalities and nonconvulsive signs and symptoms (S/Sx) of brain stem origin that culminate in generalized seizures, loss of consciousness, and postictal cardiogenic pulmonary edema. The risk of CNS-OT and its antecedent “early toxic indications” are what limits the use of hyperbaric oxygen (HBO(2)) in hyperbaric and undersea medicine. The purpose of this review is to illustrate, based on animal research, how the temporal pattern of abnormal brain stem responses that precedes an “oxtox hit” provides researchers a window into the early neurological events underlying seizure genesis. Specifically, we focus on the phenomenon of hyperoxic hyperventilation, and the medullary neurons presumed to contribute in large part to this paradoxical respiratory response; neurons in the caudal Solitary complex (cSC) of the dorsomedial medulla, including putative CO(2) chemoreceptor neurons. The electrophysiological and redox properties of O(2)-/CO(2)-sensitive cSC neurons identified in rat brain slice experiments are summarized. Additionally, evidence is summarized that supports the working hypothesis that seizure genesis originates in subcortical areas and involves cardio-respiratory centers and cranial nerve nuclei in the hind brain (brainstem and cerebellum) based on, respectively, the complex temporal pattern of abnormal cardio-respiratory responses and various nonconvulsive S/Sx that precede seizures during exposure to HBO(2).
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spelling pubmed-93606212022-08-10 The O(2)-sensitive brain stem, hyperoxic hyperventilation, and CNS oxygen toxicity Dean, Jay B. Stavitzski, Nicole M. Front Physiol Physiology Central nervous system oxygen toxicity (CNS-OT) is a complex disorder that presents, initially, as a sequence of cardio-respiratory abnormalities and nonconvulsive signs and symptoms (S/Sx) of brain stem origin that culminate in generalized seizures, loss of consciousness, and postictal cardiogenic pulmonary edema. The risk of CNS-OT and its antecedent “early toxic indications” are what limits the use of hyperbaric oxygen (HBO(2)) in hyperbaric and undersea medicine. The purpose of this review is to illustrate, based on animal research, how the temporal pattern of abnormal brain stem responses that precedes an “oxtox hit” provides researchers a window into the early neurological events underlying seizure genesis. Specifically, we focus on the phenomenon of hyperoxic hyperventilation, and the medullary neurons presumed to contribute in large part to this paradoxical respiratory response; neurons in the caudal Solitary complex (cSC) of the dorsomedial medulla, including putative CO(2) chemoreceptor neurons. The electrophysiological and redox properties of O(2)-/CO(2)-sensitive cSC neurons identified in rat brain slice experiments are summarized. Additionally, evidence is summarized that supports the working hypothesis that seizure genesis originates in subcortical areas and involves cardio-respiratory centers and cranial nerve nuclei in the hind brain (brainstem and cerebellum) based on, respectively, the complex temporal pattern of abnormal cardio-respiratory responses and various nonconvulsive S/Sx that precede seizures during exposure to HBO(2). Frontiers Media S.A. 2022-07-26 /pmc/articles/PMC9360621/ /pubmed/35957982 http://dx.doi.org/10.3389/fphys.2022.921470 Text en Copyright © 2022 Dean and Stavitzski. https://creativecommons.org/licenses/by/4.0/This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
spellingShingle Physiology
Dean, Jay B.
Stavitzski, Nicole M.
The O(2)-sensitive brain stem, hyperoxic hyperventilation, and CNS oxygen toxicity
title The O(2)-sensitive brain stem, hyperoxic hyperventilation, and CNS oxygen toxicity
title_full The O(2)-sensitive brain stem, hyperoxic hyperventilation, and CNS oxygen toxicity
title_fullStr The O(2)-sensitive brain stem, hyperoxic hyperventilation, and CNS oxygen toxicity
title_full_unstemmed The O(2)-sensitive brain stem, hyperoxic hyperventilation, and CNS oxygen toxicity
title_short The O(2)-sensitive brain stem, hyperoxic hyperventilation, and CNS oxygen toxicity
title_sort o(2)-sensitive brain stem, hyperoxic hyperventilation, and cns oxygen toxicity
topic Physiology
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9360621/
https://www.ncbi.nlm.nih.gov/pubmed/35957982
http://dx.doi.org/10.3389/fphys.2022.921470
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