(Stroke. 2001;32:925.)
© 2001 American Heart Association, Inc.
Original Contributions |
From the Neuroscience Program (S.-P.L.) and Departments of Biostatistics (J.P.M.), Internal Medicine (J.J.H.A.), Pediatric Neurology (J.J.N.), and Radiology (J.J.H.A., J.J.N.), Washington University School of Medicine, St Louis, Mo, and the Department of Chemistry (S.-K.S., J.J.H.A.), Washington University, St Louis, Mo.
Correspondence to Jeffrey J. Neil, Biomedical MR Laboratory, Washington University School of Medicine, 4525 Scott Ave, Room 2313, St Louis, MO 63110. E-mail neil{at}wuchem.wustl.edu
Background and Purpose23Na MRI may offer new insight into the evaluation of tissue injury. We performed a direct, longitudinal, morphological comparison of 1H T2 relaxation, 1H apparent diffusion coefficient (ADC), 23Na content, and histopathology after cerebral ischemia to address the hypotheses that (a) 23Na MRI is unique in comparison to 1H MRI, and (b) accumulation of 23Na is an unambiguous marker for dead tissue.
MethodsRats underwent 30 minutes of focal ischemia. MRIs of 1H T2, 1H ADC, and 23Na content were acquired from 12 hours up to 1, 2, or 14 days after reperfusion. On excision, brains were stained with triphenyltetrazolium chloride (TTC).
ResultsIn all cases, the region of abnormality increased in size for 2 days. On day 5, both 1H T2 and ADC temporarily appeared normal despite the presence of TTC-defined infarction. By comparison, the volume of tissue exhibiting abnormally intense 23Na signal mirrored the TTC-defined infarct at all time points.
ConclusionsRegions of high 23Na content correlate well with the TTC-defined infarct and may be a quantitative in vivo marker for dead tissue. In contrast, the dynamics of the 1H T2 and ADC make it difficult to interpret these images without additional information because they may appear normal despite infarction. Neither type of 1H image delineates dead tissue, and none of these methods predicts the potential infarct size at early time points.
Key Words: animal models magnetic resonance imaging sodium stroke, experimental rats
This article has been cited by other articles:
![]() |
S. C. Jones, A. Kharlamov, B. Yanovski, D. K. Kim, K. A. Easley, V. E. Yushmanov, S. K. Ziolko, and F. E. Boada Stroke Onset Time Using Sodium MRI in Rat Focal Cerebral Ischemia Stroke, March 1, 2006; 37(3): 883 - 888. [Abstract] [Full Text] [PDF] |
||||
![]() |
J. Chen, S.-K. Song, W. Liu, M. McLean, J. S. Allen, J. Tan, S. A. Wickline, and X. Yu Remodeling of cardiac fiber structure after infarction in rats quantified with diffusion tensor MRI Am J Physiol Heart Circ Physiol, August 7, 2003; 285(3): H946 - H954. [Abstract] [Full Text] [PDF] |
||||
![]() |
X. Wang, L. Xu, H. Wang, P. R. Young, M. Gaestel, and G. Z. Feuerstein Mitogen-activated Protein Kinase-activated Protein (MAPKAP) Kinase 2 Deficiency Protects Brain from Ischemic Injury in Mice J. Biol. Chem., November 8, 2002; 277(46): 43968 - 43972. [Abstract] [Full Text] [PDF] |
||||
![]() |
R. C. McKinstry, J. H. Miller, A. Z. Snyder, A. Mathur, G. L. Schefft, C. R. Almli, J. S. Shimony, S. I. Shiran, and J. J. Neil A prospective, longitudinal diffusion tensor imaging study of brain injury in newborns Neurology, September 24, 2002; 59(6): 824 - 833. [Abstract] [Full Text] [PDF] |
||||
|
Stroke Home | Subscriptions | Archives | Feedback | Authors | Help | AHA Journals Home | Search Copyright © 2001 American Heart Association, Inc. All rights reserved. Unauthorized use prohibited. |