Effects of striatal nitric oxide production on regional cerebral blood flow and seizure development in rats exposed to extreme hyperoxia.

dc.contributor.author

Gasier, Heath G

dc.contributor.author

Demchenko, Ivan T

dc.contributor.author

Allen, Barry W

dc.contributor.author

Piantadosi, Claude A

dc.date.accessioned

2021-12-21T21:02:22Z

dc.date.available

2021-12-21T21:02:22Z

dc.date.issued

2015-12

dc.date.updated

2021-12-21T21:02:22Z

dc.description.abstract

The endogenous vasodilator and signaling molecule nitric oxide has been implicated in cerebral hyperemia, sympathoexcitation, and seizures induced by hyperbaric oxygen (HBO2) at or above 3 atmospheres absolute (ATA). It is unknown whether these events in the onset of central nervous system oxygen toxicity originate within specific brain structures and whether blood flow is diverted to the brain from peripheral organs with high basal flow, such as the kidney. To explore these questions, total and regional cerebral blood flow (CBF) were measured in brain structures of the central autonomic network in anesthetized rats in HBO2 at 6 ATA. Electroencephalogram (EEG) recordings, cardiovascular hemodynamics, and renal blood flow (RBF) were also monitored. As expected, mean arterial blood pressure and total and regional CBF increased preceding EEG spikes while RBF was unaltered. Of the brain structures examined, the earliest rise in CBF occurred in the striatum, suggesting increased neuronal activation. Continuous unilateral or bilateral striatal infusion of the nitric oxide synthase inhibitor N(ω)-nitro-L-arginine methyl ester attenuated CBF responses in that structure, but global EEG discharges persisted and did not differ from controls. Our novel findings indicate that: 1) cerebral hyperemia in extreme HBO2 in rats does not occur at the expense of renal perfusion, highlighting the remarkable autoregulatory capability of the kidney, and 2) in spite of a sentinel increase in striatal blood flow, additional brain structure(s) likely govern the pathogenesis of HBO2-induced seizures because EEG discharge latency was unchanged by local blockade of striatal nitric oxide production and concomitant hyperemia.

dc.identifier

japplphysiol.00432.2015

dc.identifier.issn

8750-7587

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1522-1601

dc.identifier.uri

https://hdl.handle.net/10161/24105

dc.language

eng

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American Physiological Society

dc.relation.ispartof

Journal of applied physiology (Bethesda, Md. : 1985)

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10.1152/japplphysiol.00432.2015

dc.subject

Neostriatum

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Autonomic Nervous System

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Animals

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Rats

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Rats, Sprague-Dawley

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Seizures

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Hyperoxia

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Nitric Oxide

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NG-Nitroarginine Methyl Ester

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Enzyme Inhibitors

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Electroencephalography

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Hyperbaric Oxygenation

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Cerebrovascular Circulation

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Renal Circulation

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Male

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Nitric Oxide Synthase Type I

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Hemodynamics

dc.title

Effects of striatal nitric oxide production on regional cerebral blood flow and seizure development in rats exposed to extreme hyperoxia.

dc.type

Journal article

duke.contributor.orcid

Gasier, Heath G|0000-0001-5895-4542

pubs.begin-page

1282

pubs.end-page

1288

pubs.issue

11

pubs.organisational-group

School of Medicine

pubs.organisational-group

Pathology

pubs.organisational-group

Medicine, Pulmonary, Allergy, and Critical Care Medicine

pubs.organisational-group

Duke

pubs.organisational-group

Clinical Science Departments

pubs.organisational-group

Medicine

pubs.organisational-group

Anesthesiology

pubs.publication-status

Published

pubs.volume

119

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