Baroreceptor afferents modulate brain excitation and influence susceptibility to toxic effects of hyperbaric oxygen.
Date
2014-09
Journal Title
Journal ISSN
Volume Title
Repository Usage Stats
views
downloads
Citation Stats
Abstract
Unexplained adjustments in baroreflex sensitivity occur in conjunction with exposures to potentially toxic levels of hyperbaric oxygen. To investigate this, we monitored central nervous system, autonomic and cardiovascular responses in conscious and anesthetized rats exposed to hyperbaric oxygen at 5 and 6 atmospheres absolute, respectively. We observed two contrasting phases associated with time-dependent alterations in the functional state of the arterial baroreflex. The first phase, which conferred protection against potentially neurotoxic doses of oxygen, was concurrent with an increase in baroreflex sensitivity and included decreases in cerebral blood flow, heart rate, cardiac output, and sympathetic drive. The second phase was characterized by baroreflex impairment, cerebral hyperemia, spiking on the electroencephalogram, increased sympathetic drive, parasympatholysis, and pulmonary injury. Complete arterial baroreceptor deafferentation abolished the initial protective response, whereas electrical stimulation of intact arterial baroreceptor afferents prolonged it. We concluded that increased afferent traffic attributable to arterial baroreflex activation delays the development of excessive central excitation and seizures. Baroreflex inactivation or impairment removes this protection, and seizures may follow. Finally, electrical stimulation of intact baroreceptor afferents extends the normal delay in seizure development. These findings reveal that the autonomic nervous system is a powerful determinant of susceptibility to sympathetic hyperactivation and seizures in hyperbaric oxygen and the ensuing neurogenic pulmonary injury.
Type
Department
Description
Provenance
Citation
Permalink
Published Version (Please cite this version)
Publication Info
Demchenko, Ivan T, Heath G Gasier, Sergei Yu Zhilyaev, Alexander N Moskvin, Alexander I Krivchenko, Claude A Piantadosi and Barry W Allen (2014). Baroreceptor afferents modulate brain excitation and influence susceptibility to toxic effects of hyperbaric oxygen. Journal of applied physiology (Bethesda, Md. : 1985), 117(5). pp. 525–534. 10.1152/japplphysiol.00435.2014 Retrieved from https://hdl.handle.net/10161/24108.
This is constructed from limited available data and may be imprecise. To cite this article, please review & use the official citation provided by the journal.
Collections
Scholars@Duke
Heath Gasier
Dr. Gasier is a physiologist and nutritionist. His research is focused on understanding how breathing altered PO2 impacts cell physiology in the lung, brain, and skeletal muscle. Emphasis is placed on mitochondrial quality control (dynamics, mitophagy, and biogenesis) and bioenergetics. He uses in vivo and in vitro models, and employs an array of methods (e.g., confocal and electron microscopy, Seahorse respiration, immunoblotting, RT-qPCR, ELISA’s, isotope tracers, and 10X genomics) for hypothesis testing. The goal of his research is to improve the operational capacity of divers and safety of hyperoxia in hyperbaric and critical care medicine. Dr. Gasier believes in a hands-on mentoring approach and individualized training plans based on mentee’s aspirations. He is committed to lifetime learning and contributing to knowledge advancement.
Claude Anthony Piantadosi
Dr. Piantadosi's laboratory has special expertise in the pathogenic mechanisms of acute organ failure, particularly acute lung injury (ALI), with an emphasis on the molecular regulatory roles of the physiological gases— oxygen, carbon monoxide, and nitric oxide— as they relate to the damage responses to acute inflammation. The basic science focuses on oxidative processes and redox-regulation, especially the molecular mechanisms by which reactive oxygen and nitrogen species transmit biological signals involved in the maintenance of energy metabolism and mitochondrial health, but also contribute to pathogenesis and to the resolution of tissue injury.
Clinically, ALI and the related syndrome of multiple organ failure has a high mortality, which is related to the host inflammatory response, but is not well understood scientifically; thus, the laboratory is devoted to understanding these mechanisms in the context of the host response to relevant but well-controlled experimental manipulations including hyperoxia, bacterial infections, toxic drugs, and cytokine/chemokine signals. The approach relies on animal models, mainly transgenic and knockout mice, and cell models, especially lung and heart cells to evaluate and understand the physiology, pathology, and cell and molecular biology of the injury responses, to test independent and integrated mechanisms, and to devise interventions to prevent damage.
Apart from the lung, significant work is devoted to understanding damage to the heart, brain, liver, and kidney caused by these immune mechanisms, specifically emphasizing the role of mitochondria, key targets and sources of oxidative damage. This damage compromises their ability to support energy homeostasis and advanced cellular functions, and impacts on the important roles these organelles play in cell death by apoptosis and necrosis as well as in the resolution of cellular damage and inflammation.
Barry W. Allen
Employing the techniques of analytical electrochemistry, in vitro and in vivo, to elucidate the physiological roles of diffusible signaling molecules in brain, in other excitable tissues, and in blood. Such molecules include Ca++, NO·, and CO.
Unless otherwise indicated, scholarly articles published by Duke faculty members are made available here with a CC-BY-NC (Creative Commons Attribution Non-Commercial) license, as enabled by the Duke Open Access Policy. If you wish to use the materials in ways not already permitted under CC-BY-NC, please consult the copyright owner. Other materials are made available here through the author’s grant of a non-exclusive license to make their work openly accessible.