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J Cereb Blood Flow Metab. 2019 Jul;39(7):1232-1246. doi: 10.1177/0271678X17752795. Epub 2018 Jan 19.

Posterior reversible encephalopathy syndrome in stroke-prone spontaneously hypertensive rats on high-salt diet.

Author information

1
1 Department of Radiology, Neurovascular Research Laboratory, Massachusetts General Hospital and Harvard Medical School, Charlestown, MA, USA.
2
2 Athinoula A. Martinos Center for Biomedical Imaging, Department of Radiology, Massachusetts General Hospital and Harvard Medical School, Charlestown, MA, USA.
3
3 Emergency Headache Center, Department of Neurology, Lariboisière Hospital, APHP, Sorbonne Paris-Cité, Paris, France.
4
4 Department of Ocean and Mechanical Engineering, Florida Atlantic University, Boca Raton, FL USA.
5
5 Department of Neurological Sciences, University of Vermont, Burlington, VT, USA.
6
6 J. Philip Kistler Stroke Research Center, Department of Neurology, Massachusetts General Hospital and Harvard Medical School, Boston, MA, USA.
7
7 Department of Neurology, Stroke Service, Massachusetts General Hospital and Harvard Medical School, Boston, MA, USA.

Abstract

Stroke-prone spontaneously hypertensive rats (SHRSP) on high-salt diet are characterized by extremely high arterial pressures, and have been endorsed as a model for hypertensive small vessel disease and vascular cognitive impairment. However, rapidly developing malignant hypertension is a well-known cause of posterior reversible encephalopathy syndrome (PRES) in humans, associated with acute neurological deficits, seizures, vasogenic cerebral edema and microhemorrhages. In this study, we aimed to examine the overlap between human PRES and SHRSP on high-salt diet. In SHRSP, arterial blood pressure progressively increased after the onset of high-salt diet and seizure-like signs emerged within three to five weeks. MRI revealed progressive T2-hyperintense lesions suggestive of vasogenic edema predominantly in the cortical watershed and white matter regions. Histopathology confirmed severe blood-brain barrier disruption, white matter vacuolization and microbleeds that were more severe posteriorly. Hematological data suggested a thrombotic microangiopathy as a potential underlying mechanism. Unilateral common carotid artery occlusion protected the ipsilateral hemisphere from neuropathological abnormalities. Notably, all MRI and histopathological abnormalities were acutely reversible upon switching to regular diet and starting antihypertensive treatment. Altogether our data suggest that SHRSP on high-salt diet recapitulates the neurological, histopathological and imaging features of human PRES rather than chronic progressive small vessel disease.

KEYWORDS:

Animal models; cerebral blood flow; hypertension; posterior cerebral reversible encephalopathy; white matter

PMID:
29350576
PMCID:
PMC6668522
[Available on 2020-07-01]
DOI:
10.1177/0271678X17752795

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