Blood-Brain Barrier Disruption as a Potential Target for Therapy in Posterior Reversible Encephalopathy Syndrome: Evidence From Multimodal MRI in Rats.

Quanlai Wang,Zheng Chen,Yu Zeng,Chunqiang Lu,Alexander Lerner,Guiquan Shen,Bo Gao,Bin Huang

doi:10.3389/fneur.2019.01211

Abstract

Background: To explore blood–brain barrier disruption in hypertensive posterior reversible encephalopathy syndrome.Methods: The hypertension rat models were successfully established and scanned on 7T micro-MRI. MRI parameter maps including apparent diffusion coefficient, T1 value, and perfusion metrics such as cerebral blood volume, cerebral blood flow, mean transit time and time to peak maps, were calculated.Results: The ADC values of the experimental group were higher than those of the control group both in cortical (P < 0.01) and subcortical (P < 0.05) regions. Voxel-wise analysis of ADC maps localized vasogenic edema primarily to the posterior portion of the brain. The increase in cerebral blood volume and cerebral blood flow values were found in the cortical and subcortical regions of rats with acute hypertension. No correlation was found between perfusion metrics and mean arterial pressure. The Evans blue dye content was higher in the posterior brain region than the anterior one (P < 0.05).Conclusions: Cerebral vasogenic edema resulting from acute hypertension supports the hypothesis of posterior reversible encephalopathy syndrome as the result of blood–brain barrier disruption, which maybe the potential therapeutic target for intervention.

Highlights

Posterior reversible encephalopathy syndrome (PRES) usually occurs following a precipitous rise of blood pressure [1]
One of the possible inciting factors is the rapid rise in blood pressure, which exceeds the upper limit of cerebral autoregulation, and results in excessive blood flow with subsequent blood– brain barrier (BBB) breakdown
The aim of the present study is to investigate whether cerebral edema, hemodynamic change, and BBB disruption can be detected in rat model using 7.0 T micro-MRI and to elucidate the pathophysiological mechanism of PRES

Summary

Introduction

Posterior reversible encephalopathy syndrome (PRES) usually occurs following a precipitous rise of blood pressure [1]. Acute hypertension may lead to persistent and severe disorder of cerebral circulation with passively or forced dilation of the cerebral arterioles, resulting in cerebral hyperperfusion, brain edema, and increased intracranial pressure [2, 3]. One of the possible inciting factors is the rapid rise in blood pressure, which exceeds the upper limit of cerebral autoregulation, and results in excessive blood flow with subsequent blood– brain barrier (BBB) breakdown. Severe hypertension may lead to excessive reaction of the cerebrovascular autoregulation, spasm of small cerebral vessels, and decrease in perfusion, resulting in ischemia, BBB disruption, increased vascular permeability, and brain edema [10]. The aim of the present study is to investigate whether cerebral edema, hemodynamic change, and BBB disruption can be detected in rat model using 7.0 T micro-MRI and to elucidate the pathophysiological mechanism of PRES. To explore blood–brain barrier disruption in hypertensive posterior reversible encephalopathy syndrome

Objectives

Methods

Results

Conclusion