Trial of the cerebral perfusion response to sodium nitrite infusion in patients with acute subarachnoid haemorrhage using arterial spin labelling MRI.

Autor: Ezra M; Nuffield Division of Anaesthetics, Nuffield Department of Clinical Neurosciences, University of Oxford, Oxford, UK. Electronic address: martyn.ezra@ndcn.ox.ac.uk., Franko E; Nuffield Division of Anaesthetics, Nuffield Department of Clinical Neurosciences, University of Oxford, Oxford, UK., Spronk DB; Nuffield Division of Anaesthetics, Nuffield Department of Clinical Neurosciences, University of Oxford, Oxford, UK., Lamb C; Neuro Intensive Care Unit, John Radcliffe Hospital, Oxford University Hospitals NHS Foundation Trust, Oxford, UK., Okell TW; Wellcome Centre for Integrative Neuroimaging, FMRIB, Nuffield Department of Clinical Neurosciences, University of Oxford, Oxford, UK., Pattinson KT; Nuffield Division of Anaesthetics, Nuffield Department of Clinical Neurosciences, University of Oxford, Oxford, UK.
Jazyk: angličtina
Zdroj: Nitric oxide : biology and chemistry [Nitric Oxide] 2024 Oct 05; Vol. 153, pp. 50-60. Date of Electronic Publication: 2024 Oct 05.
DOI: 10.1016/j.niox.2024.10.003
Abstrakt: Aneurysmal subarachnoid haemorrhage (SAH) is a devastating subset of stroke. One of the major determinants of outcome is an evolving multifactorial injury occurring in the first 72 hours, known as early brain injury. Reduced nitric oxide (NO) bioavailability and an associated disruption to cerebral perfusion is believed to play an important role in this process. We sought to explore this relationship, by examining the effect on cerebral perfusion of the in vivo manipulation of NO levels using an exogenous NO donor (sodium nitrite). We performed a double blind placebo controlled randomised experimental medicine study of the cerebral perfusion response to sodium nitrite infusion during the early brain injury period in 15 low grade (World Federation of Neurosurgeons grade 1-2) SAH patients. Patients were randomly assigned to receive sodium nitrite at 10 mcg/kg/min or saline placebo. Assessment occurred following endovascular aneurysm occlusion, mean time after ictus 66h (range 34-90h). Cerebral perfusion was quantified before infusion commencement and after 3 hours, using multi-post labelling delay (multi-PLD) vessel encoded pseudocontinuous arterial spin labelling (VEPCASL) magnetic resonance imaging (MRI). Administration of sodium nitrite was associated with a significant increase in average grey matter cerebral perfusion. Group level voxelwise analysis identified that increased perfusion occurred within regions of the brain known to exhibit enhanced vulnerability to injury. These findings highlight the role of impaired NO bioavailability in the pathophysiology of early brain injury.
(Copyright © 2024 The Authors. Published by Elsevier Inc. All rights reserved.)
Databáze: MEDLINE
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