Influence of simultaneous pressor and vasodilatory agents on the evolution of infarct growth in experimental acute middle cerebral artery occlusion.
Animals
Collateral Circulation
/ drug effects
Diffusion Magnetic Resonance Imaging
/ methods
Dogs
Drug Therapy, Combination
/ methods
Hydralazine
/ pharmacology
Infarction, Middle Cerebral Artery
/ diagnostic imaging
Ischemic Stroke
/ diagnostic imaging
Magnetic Resonance Angiography
/ methods
Norepinephrine
/ pharmacology
Treatment Outcome
Vasoconstrictor Agents
/ pharmacology
Vasodilator Agents
/ pharmacology
MRI
angiography
brain
stroke
Journal
Journal of neurointerventional surgery
ISSN: 1759-8486
Titre abrégé: J Neurointerv Surg
Pays: England
ID NLM: 101517079
Informations de publication
Date de publication:
Aug 2021
Aug 2021
Historique:
received:
22
06
2020
revised:
13
08
2020
accepted:
16
08
2020
pubmed:
10
9
2020
medline:
27
7
2021
entrez:
9
9
2020
Statut:
ppublish
Résumé
This study sought to test the hypothesis that simultaneous central blood pressure elevation and potent vasodilation can mitigate pial collateral-dependent infarct growth in acute ischemic stroke. Twenty mongrel canines (20-30 kg) underwent permanent middle cerebral artery occlusion (MCAO). Eight subjects received continuous infusion of norepinephrine (0.1-1.5200 µg/kg/min; titrated to a median of 34 mmHg above baseline mean arterial pressure) and hydralazine (20 mg) starting 30 min following MCAO. Pial collateral recruitment was scored prior to treatment and used to predict infarct volume based on a previously reported parameterization. Serial diffusion magnetic resonance imaging (MRI) acquisitions tracked infarct volumes over a 4-hour time frame. Infarct volumes and infarct volume growth between treatment and control groups were compared with each other and to predicted values. Fluid-attenuated inversion recovery (FLAIR) MRI, susceptibility weighted imaging (SWI), and necropsy findings were included in the evaluation. Differences between treatment and control group varied by pial collateral recruitment based on indicator-variable regression effects analysis with interaction confirmed by regression model fit. Benefit in treatment group was only in subjects with poor collaterals which had 35.7% less infarct volume growth (P=0.0008; ANOVA) relative to controls. Measured infarct growth was significantly lower than predicted by the model (linear regression partial F-test, slope P<0.001, intercept=0.003). There was no evidence for cerebral hemorrhage or posterior reversible encephalopathy syndrome. Our results indicate that a combination of norepinephrine and hydralazine administered in the acute phase of ischemic stroke mitigates infarct evolution in subjects with poor but not good collateral recruitment.
Sections du résumé
BACKGROUND
BACKGROUND
This study sought to test the hypothesis that simultaneous central blood pressure elevation and potent vasodilation can mitigate pial collateral-dependent infarct growth in acute ischemic stroke.
METHODS
METHODS
Twenty mongrel canines (20-30 kg) underwent permanent middle cerebral artery occlusion (MCAO). Eight subjects received continuous infusion of norepinephrine (0.1-1.5200 µg/kg/min; titrated to a median of 34 mmHg above baseline mean arterial pressure) and hydralazine (20 mg) starting 30 min following MCAO. Pial collateral recruitment was scored prior to treatment and used to predict infarct volume based on a previously reported parameterization. Serial diffusion magnetic resonance imaging (MRI) acquisitions tracked infarct volumes over a 4-hour time frame. Infarct volumes and infarct volume growth between treatment and control groups were compared with each other and to predicted values. Fluid-attenuated inversion recovery (FLAIR) MRI, susceptibility weighted imaging (SWI), and necropsy findings were included in the evaluation.
RESULTS
RESULTS
Differences between treatment and control group varied by pial collateral recruitment based on indicator-variable regression effects analysis with interaction confirmed by regression model fit. Benefit in treatment group was only in subjects with poor collaterals which had 35.7% less infarct volume growth (P=0.0008; ANOVA) relative to controls. Measured infarct growth was significantly lower than predicted by the model (linear regression partial F-test, slope P<0.001, intercept=0.003). There was no evidence for cerebral hemorrhage or posterior reversible encephalopathy syndrome.
CONCLUSION
CONCLUSIONS
Our results indicate that a combination of norepinephrine and hydralazine administered in the acute phase of ischemic stroke mitigates infarct evolution in subjects with poor but not good collateral recruitment.
Identifiants
pubmed: 32900906
pii: neurintsurg-2020-016539
doi: 10.1136/neurintsurg-2020-016539
doi:
Substances chimiques
Vasoconstrictor Agents
0
Vasodilator Agents
0
Hydralazine
26NAK24LS8
Norepinephrine
X4W3ENH1CV
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
741-745Subventions
Organisme : NINDS NIH HHS
ID : R01 NS093908
Pays : United States
Informations de copyright
© Author(s) (or their employer(s)) 2021. No commercial re-use. See rights and permissions. Published by BMJ.
Déclaration de conflit d'intérêts
Competing interests: None declared.