Circulating bacterial lipopolysaccharide-induced inflammation reduces flow in brain-irrigating arteries independently from cerebrovascular prostaglandin production.
Neuroscience. 2017-03-01; 346: 160-172
DOI: 10.1016/j.neuroscience.2017.01.018
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1. Neuroscience. 2017 Mar 27;346:160-172. doi: 10.1016/j.neuroscience.2017.01.018.
Epub 2017 Jan 23.
Circulating bacterial lipopolysaccharide-induced inflammation reduces flow in
brain-irrigating arteries independently from cerebrovascular prostaglandin
production.
Villéga F(1), Delpech JC(2), Griton M(3), André C(2), Franconi JM(4), Miraux
S(4), Konsman JP(5).
Author information:
(1)Service de Neuropédiatrie, CIC-0005, Centre Hospitalier Universitaire (CHU) de
Bordeaux, Bordeaux, France; CNRS, Résonance Magnétique des Systèmes Biologiques,
UMR 5536, Bordeaux, France.
(2)Univ. Bordeaux, RMSB, UMR 5536, Bordeaux, France; CNRS,
PsychoNeuroImmunologie, Nutrition et Génétique, UMR 5226, Bordeaux, France.
(3)CNRS, Résonance Magnétique des Systèmes Biologiques, UMR 5536, Bordeaux,
France; Univ. Bordeaux, RMSB, UMR 5536, Bordeaux, France; Service de Anesthésie
Réanimation Neurochirurgicale, Centre Hospitalier Universitaire (CHU) de
Bordeaux, Bordeaux, France.
(4)CNRS, Résonance Magnétique des Systèmes Biologiques, UMR 5536, Bordeaux,
France; Univ. Bordeaux, RMSB, UMR 5536, Bordeaux, France.
(5)CNRS, Résonance Magnétique des Systèmes Biologiques, UMR 5536, Bordeaux,
France; Univ. Bordeaux, RMSB, UMR 5536, Bordeaux, France. Electronic address:
.
Brain dysfunction is a frequent complication of the systemic inflammatory
response to bacterial infection or sepsis. In the present work, the effects of
intravenous bacterial lipopolysaccharide (LPS) administration on cerebral
arterial blood flow were assessed with time-of-flight (TOF)-based magnetic
resonance angiography (MRA) in mice. Cerebral expression of the transcription
factors nuclear factor-kappaB (NF-κB) and c-Fos and that of enzymes synthesizing
vasoactive mediators, such as prostaglandins and nitric oxide, known to be
increased under inflammatory conditions, were studied in the same animals.
Time-resolved TOF MRA revealed no differences in blood flow in the internal
carotids upstream of the circle of Willis, but indicated lower flow in its
lateral parts as well as in the middle and anterior cerebral arteries after
intravenous LPS injection as compared to saline administration. Although LPS did
not increase c-Fos expression in ventral forebrain structures of these animals,
it did induce NF-κB in meningeal blood vessels. LPS also increased cerebral
expression of cyclooxygenase-2 and prostaglandin E synthase mRNAs, but de novo
expression occurred in veins rather than in arteries. In conclusion, our work
indicates that LPS-induced systemic inflammation does not necessarily affect
filling of the circle of the Willis from the periphery, but that circulating LPS
alters outflow from the circle of Willis to the middle and anterior cerebral
arteries. These modifications in arterial flow were not related to increased
cerebral synthesis of prostaglandins, but may instead be the consequence of the
action of circulating prostaglandins and other vasoactive mediators on
brain-irrigating arteries during systemic inflammation.
Copyright © 2017 IBRO. Published by Elsevier Ltd. All rights reserved.
DOI: 10.1016/j.neuroscience.2017.01.018
PMID: 28126368 [Indexed for MEDLINE]