Persistent cerebrovascular damage after stroke in type two diabetic rats measured by magnetic resonance imaging

Guangliang Ding1, Tao Yan1, Jieli Chen1

  • 1From the Department of Neurology, Henry Ford Hospital, Detroit, MI (G.D., T.Y., J.C., M.C., L.L., Q.L., C.C., R.N., Q.J.); and Department of Physics, Oakland University, Rochester, MI (M.C.).

Stroke
|December 20, 2014
PubMed
Abstract

Insights

Diabetic rats showed significantly more blood-brain barrier damage and lower axonal density after stroke compared to nondiabetic rats. MRI revealed this increased vascular damage and neuronal injury over five weeks.

Area of Science:

  • Neuroscience
  • Vascular Biology
  • Medical Imaging

Background:

  • Diabetes mellitus is a systemic disease with significant vascular implications.
  • Stroke-induced blood-brain barrier (BBB) disruption may be exacerbated in diabetic individuals.
  • Longitudinal studies on BBB changes post-stroke in diabetes are limited.

Purpose of the Study:

  • To noninvasively evaluate and compare longitudinal BBB disruption after stroke in diabetic and nondiabetic rats using Magnetic Resonance Imaging (MRI).
  • To investigate the impact of Type 2 Diabetes Mellitus (T2DM) on stroke outcomes, specifically BBB integrity and lesion development.

Main Methods:

  • Type 2 Diabetes Mellitus (T2DM) induced in Wistar rats via high-fat diet and streptozotocin.
  • Middle Cerebral Artery Occlusion (MCAO) performed on T2DM and nondiabetic wild-type (WT) rats.
  • Longitudinal MRI scans (T2 maps, contrast-enhanced T1-weighted, susceptibility-weighted imaging, diffusion fractional anisotropy) conducted weekly for 5 weeks post-MCAO.

Main Results:

  • Ischemic lesion volumes (T2 maps) did not differ significantly between T2DM and WT rats.
  • T2DM rats exhibited significantly larger volumes of BBB disruption (contrast-enhanced T1-weighted) and cerebral hemorrhage (susceptibility-weighted imaging) from 1 to 5 weeks post-stroke (P<0.05).
  • Diffusion fractional anisotropy values were significantly lower in T2DM rats, indicating reduced axonal density (P<0.03).

Conclusions:

  • Standard T2-weighted MRI did not reveal differences in ischemic lesion volume between diabetic and nondiabetic rats post-stroke.
  • Advanced MRI techniques (contrast-enhanced T1-weighted and susceptibility-weighted imaging) demonstrated significantly greater ischemic vascular damage in diabetic rats.
  • Fractional anisotropy measurements indicated lower axonal density in diabetic rats, suggesting more severe neuronal injury following stroke.

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