Changes in the cerebrospinal fluid lipid profile following subarachnoid hemorrhage in a closed cranium model: Correlations to cerebral vasospasm, neuronal cell death and Interleukin-6 synthesis. A pilot study.
Animals
Apoptosis
Basilar Artery
/ diagnostic imaging
Biomarkers
/ cerebrospinal fluid
Disease Models, Animal
Interleukin-6
/ biosynthesis
Intracranial Pressure
Lipids
/ cerebrospinal fluid
Neurons
/ metabolism
Phosphatidylcholines
/ cerebrospinal fluid
Phosphatidylethanolamines
/ cerebrospinal fluid
Pilot Projects
Rabbits
Subarachnoid Hemorrhage
/ cerebrospinal fluid
Vasoconstriction
Vasospasm, Intracranial
/ cerebrospinal fluid
Brain injury
Delayed cerebral vasospasm
Interleukin-6
Sphingolipids
Subarachnoid hemorrhage
Journal
Journal of stroke and cerebrovascular diseases : the official journal of National Stroke Association
ISSN: 1532-8511
Titre abrégé: J Stroke Cerebrovasc Dis
Pays: United States
ID NLM: 9111633
Informations de publication
Date de publication:
Sep 2020
Sep 2020
Historique:
received:
08
04
2020
revised:
03
06
2020
accepted:
10
06
2020
entrez:
19
8
2020
pubmed:
19
8
2020
medline:
3
11
2020
Statut:
ppublish
Résumé
Phospholipids and sphingolipids are cell membrane components, that participate in signaling events and regulate a wide variety of vital cellular processes. Sphingolipids are involved in ischemic stroke pathophysiology. Throughout cleavage of membrane sphingomyelin by sphingomyelinase in stroke patients, it results in increased Ceramide (Cer) levels in brain tissue. Different studies showed the evidence that sphingomyelinase with Cer production induces expression of interleukin (IL)-6 and have vasoconstrictive proprieties. With this study, we intend to evaluate cerebrospinal fluid (CSF) lipid profile changes in a rabbit closed cranium subarachnoid hemorrhage (SAH) model. A total of 14 New Zealand white rabbits were randomly allocated either to SAH or sham group. In the first group SAH was induced by extracranial-intracranial shunting from the subclavian artery into the cisterna magna. Intracranial pressure (ICP) and arterial blood pressure were continuously monitored. Digital subtraction angiography of the basilar artery, CSF and blood samples were performed at day 0 pre SAH and on day 3 post SAH. The amount of IL-6 and various lipids in CSF were quantified using ELISA and Liquid Chromatography-Mass Spectrometry respectively. Cell death was detected in bilateral basal cortex, hippocampus (CA1 and CA3) using terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL). SAH Induction led to acute increase of ICP and increased delayed cerebral vasospasm (DCVS). At follow up CSF IL-6 levels showed a significant increase compared to baseline. Between baseline and follow up there were no significant differences in any of the measured CSF Lipids irrespective of subgroups. No relevant correlation was found between IL-6 and any of the sphingolipids. We found a correlation between baseline and follow up for the phospholipids phosphatidylethanolamine and phosphatidylcholine. Neuronal apoptosis, DCVS and IL-6 seems not to be related to changes in CSF lipid profiles except for PEA and PC in a rabbit closed cranium SAH model.
Sections du résumé
BACKGROUND
BACKGROUND
Phospholipids and sphingolipids are cell membrane components, that participate in signaling events and regulate a wide variety of vital cellular processes. Sphingolipids are involved in ischemic stroke pathophysiology. Throughout cleavage of membrane sphingomyelin by sphingomyelinase in stroke patients, it results in increased Ceramide (Cer) levels in brain tissue. Different studies showed the evidence that sphingomyelinase with Cer production induces expression of interleukin (IL)-6 and have vasoconstrictive proprieties. With this study, we intend to evaluate cerebrospinal fluid (CSF) lipid profile changes in a rabbit closed cranium subarachnoid hemorrhage (SAH) model.
METHODS
METHODS
A total of 14 New Zealand white rabbits were randomly allocated either to SAH or sham group. In the first group SAH was induced by extracranial-intracranial shunting from the subclavian artery into the cisterna magna. Intracranial pressure (ICP) and arterial blood pressure were continuously monitored. Digital subtraction angiography of the basilar artery, CSF and blood samples were performed at day 0 pre SAH and on day 3 post SAH. The amount of IL-6 and various lipids in CSF were quantified using ELISA and Liquid Chromatography-Mass Spectrometry respectively. Cell death was detected in bilateral basal cortex, hippocampus (CA1 and CA3) using terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL).
RESULTS
RESULTS
SAH Induction led to acute increase of ICP and increased delayed cerebral vasospasm (DCVS). At follow up CSF IL-6 levels showed a significant increase compared to baseline. Between baseline and follow up there were no significant differences in any of the measured CSF Lipids irrespective of subgroups. No relevant correlation was found between IL-6 and any of the sphingolipids. We found a correlation between baseline and follow up for the phospholipids phosphatidylethanolamine and phosphatidylcholine.
CONCLUSIONS
CONCLUSIONS
Neuronal apoptosis, DCVS and IL-6 seems not to be related to changes in CSF lipid profiles except for PEA and PC in a rabbit closed cranium SAH model.
Identifiants
pubmed: 32807460
pii: S1052-3057(20)30472-9
doi: 10.1016/j.jstrokecerebrovasdis.2020.105054
pii:
doi:
Substances chimiques
Biomarkers
0
Interleukin-6
0
Lipids
0
Phosphatidylcholines
0
Phosphatidylethanolamines
0
phosphatidylethanolamine
39382-08-6
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
105054Informations de copyright
Copyright © 2020 Elsevier Inc. All rights reserved.
Déclaration de conflit d'intérêts
Declaration of Competing Interest The current project has been financially supported by a grant from the Research Fund of the Kantonsspital Aarau, Switzerland. The project has been awarded and funded by the Synthes Research Award of the Swiss Neurosurgical Society. The authors have no financial or other conflict of interest to declare.