This Article Full Text Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Lee, V. M. Articles by Watson, B. Search for Related Content PubMed PubMed Citation Articles by Lee, V. M. Articles by Watson, B.

(Stroke. 1996;27:2110-2119.)
© 1996 American Heart Association, Inc.

Articles

Evolution of Photochemically Induced Focal Cerebral Ischemia in the Rat

Magnetic Resonance Imaging and Histology

Vee Meng Lee, PhD; Newman G. Burdett, PhD; T. Adrian Carpenter, PhD; Laurance D. Hall, PhD; Perouz S. Pambakian, BSc; Sara Patel, PhD; Nigel I. Wood, MSc Michael F. James, PhD

the Herchel Smith Laboratory (V.M.L., N.G.B., T.A.C., L.D.H.), Cambridge University School of Clinical Medicine, Cambridge, and SmithKline Beecham Pharmaceuticals (P.S.P., S.P., N.I.W., M.F.J.), Harlow, Essex, United Kingdom.

Correspondence to Dr M.F. James, SmithKline Beecham Pharmaceuticals, New Frontiers Science Park (North), Third Ave, Harlow, Essex CM19 5AW, UK. E-mail Michael_F_James@sbphrd.com.

Background and Purpose Magnetic resonance imaging (MRI) is increasingly used to study the pathophysiological evolution of cerebral ischemia in humans and animals. We have investigated photochemically induced (rose bengal) focal cerebral ischemia, a relatively noninvasive, reproducible model for stroke, and compared the evolution of the ischemic response in vivo and postmortem with MRI and histology, respectively.

Methods MR images weighted for T₂, diffusion, and T₂* and parallel histological sections stained with cresyl fast violet (CFV) and for glial fibrillary acid protein were obtained from 34 adult male Hooded Lister rats at seven time points (3.75 to 196 hours) after bilateral ischemia induction. From CFV histology, lesion volumes and cell counts were calculated; from diffusion-weighted and T₂-weighted images, apparent diffusion coefficients and lesion volumes were determined.

Results Both MRI and histology revealed a well-defined lesion at 3.75 hours after irradiation and a consistent pattern of temporal evolution; lesion apparent diffusion coefficients decreased significantly by 3.75 hours, increased significantly by day 2, and correlated strikingly with the decline in lesion CFV-positive cell numbers. After day 2, astrocytes and connective tissue cells invaded the infarct. Throughout the time course, lesion volumes determined in vivo and postmortem (after shrinkage correction) agreed well.

Conclusions MRI changes quantitatively reflect histopathology, revealing reproducible primary and secondary damage characteristics noninvasively. These changes essentially replicate those reported for other animal stroke models and clinically, emphasizing the value both of MRI and the photochemically induced focal cerebral ischemia model in stroke research.

Editorial Comment

Magnetic Resonance Imaging and Histology

Brant Watson, PhD, Guest Editor

Department of Neurologyand Cerebral Vascular Disease Research Center, University of Miami School of Medicine, Miami, Fla