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对氧敏感的脑干、高氧性过度通气与中枢神经系统氧中毒

The O-sensitive brain stem, hyperoxic hyperventilation, and CNS oxygen toxicity.

作者信息

Dean Jay B, Stavitzski Nicole M

机构信息

Department of Molecular Pharmacology and Physiology, University of South Florida, Tampa, FL, United States.

出版信息

Front Physiol. 2022 Jul 26;13:921470. doi: 10.3389/fphys.2022.921470. eCollection 2022.

DOI:10.3389/fphys.2022.921470
PMID:35957982
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9360621/
Abstract

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) 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 chemoreceptor neurons. The electrophysiological and redox properties of O-/CO-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.

摘要

中枢神经系统氧中毒(CNS - OT)是一种复杂的病症,最初表现为一系列心肺异常以及源自脑干的非惊厥性体征和症状,最终发展为全身性癫痫发作、意识丧失和发作后心源性肺水肿。CNS - OT的风险及其先前的“早期中毒指征”限制了高压氧(HBO)在高压和水下医学中的应用。本综述的目的是基于动物研究,阐述在“氧中毒发作”之前脑干异常反应的时间模式如何为研究人员提供一个窗口,以了解癫痫发作起源的早期神经学事件。具体而言,我们关注高氧性过度通气现象,以及被认为在很大程度上导致这种矛盾性呼吸反应的延髓神经元;即延髓背内侧尾侧孤束复合体(cSC)中的神经元,包括假定的CO化学感受器神经元。总结了在大鼠脑片实验中鉴定出的对O⁻/CO敏感的cSC神经元的电生理和氧化还原特性。此外,基于在HBO暴露期间癫痫发作之前异常心肺反应的复杂时间模式以及各种非惊厥性体征和症状,总结了支持癫痫发作起源于皮层下区域并涉及后脑(脑干和小脑)中的心肺中心和颅神经核这一工作假设的证据。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cc26/9360621/0587521b5e61/fphys-13-921470-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cc26/9360621/fcde79890597/fphys-13-921470-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cc26/9360621/97c3bde4ae95/fphys-13-921470-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cc26/9360621/b922b356f6e6/fphys-13-921470-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cc26/9360621/0587521b5e61/fphys-13-921470-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cc26/9360621/fcde79890597/fphys-13-921470-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cc26/9360621/97c3bde4ae95/fphys-13-921470-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cc26/9360621/b922b356f6e6/fphys-13-921470-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cc26/9360621/0587521b5e61/fphys-13-921470-g004.jpg

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