Perfusion Deficit Parallels Exacerbation of Cerebral Ischemia/Reperfusion Injury in Hyperglycemic Rats

Author:

Quast Michael J.123,Wei Jingna1,Huang Neng C.4,Brunder Donald G.5,Sell Stacy L.12,Gonzalez Jose M.1,Hillman Gilbert R.6,Kent Thomas A.267

Affiliation:

1. Department of Marine Biomedical Institute, University of Texas Medical Branch, Galveston, Texas

2. Department of Anatomy and Neurosciences, University of Texas Medical Branch, Galveston, Texas

3. Department of Radiology, University of Texas Medical Branch, Galveston, Texas

4. Division of Medical Physics, Nathan Kline Institute, Orangeburg, NY, U.S.A.

5. Information Services, University of Texas Medical Branch, Galveston, Texas

6. Department of Pharmacology, University of Texas Medical Branch, Galveston, Texas

7. Department of Neurology, University of Texas Medical Branch, Galveston, Texas

Abstract

Magnetic resonance imaging (MRI) techniques were used to determine the effect of preexisting hyperglycemia on the extent of cerebral ischemia/reperfusion injury and the level of cerebral perfusion. Middle cerebral artery occlusion (MCAO) was induced by a suture insertion technique. Forty one rats were divided into hyperglycemic and normoglycemic groups with either 4 hours of continuous MCAO or 2 hours of MCAO followed by 2 hours of reperfusion. Diffusion-weighted imaging (DWI) was performed at 4 hours after MCAO to quantify the degree of injury in 6 brain regions. Relative cerebral blood flow (CBF) and cerebral blood volume (CBV) were estimated using gradient echo (GE) bolus tracking and steady-state spin echo (SE) imaging techniques, respectively. Brain injury correlated with the perfusion level measured in both SE CBV and dynamic GE CBF images. In the temporary MCAO model, mean lesion size in DWI was 118% larger and hemispheric CBV was reduced by 37% in hyperglycemic compared with normoglycemic rats. Hyperglycemia did not significantly exacerbate brain injury or CBV deficit in permanent MCAO models. We conclude that preexisting hyperglycemia increases acute postischemic MRI-measurable brain cellular injury in proportion to an associated increased microvascular ischemia.

Publisher

SAGE Publications

Subject

Cardiology and Cardiovascular Medicine,Clinical Neurology,Neurology

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