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(Stroke. 2001;32:2615.)
© 2001 American Heart Association, Inc.

Original Contributions

A New Model of Localized Ischemia in Rat Somatosensory Cortex Produced by Cortical Compression

Shigeru Watanabe, MD; John R. Hoffman, PhD; Rebecca L. Craik, PhD; Peter J. Hand, VMD, PhD; Sidney E. Croul, MD; Martin Reivich, MD Joel H. Greenberg, PhD

From the Cerebrovascular Research Center, Department of Neurology, University of Pennsylvania School of Medicine, Philadelphia (S.W., M.R., J.H.G.); Department of Animal Biology, School of Veterinary Medicine, University of Pennsylvania, Philadelphia (P.J.H.); Departments of Biology (J.R.H.) and Physical Therapy (R.L.C.), Arcadia University, Glenside, Pa; and Department of Pathology, MCP-Hahnemann University, Philadelphia, Pa (S.E.C.).

Correspondence to Joel H. Greenberg, PhD, Cerebrovascular Research Center, 415 Stemmler Hall, 3450 Hamilton Walk, University of Pennsylvania, Philadelphia, PA 19104-6063. E-mail greenberg{at}cvrc.med.upenn.edu

Background and Purpose—— Because of its precise connectivity and functional specificity, the rat whisker-barrel system offers an excellent opportunity to study experience-dependent neuroplasticity. However, data are lacking regarding the neuroplasticity of this system after cerebral ischemia. The purpose of the present study was to develop a reproducible model for the production of ischemia/reperfusion of the posteromedial barrel subfield (PMBSF) in the rat, which is the visible representation of the large whiskers on the opposite face.

Methods—— Focal cortical ischemia was induced in male Sprague-Dawley rats (n=40) by slowly compressing the intact dura (maximum 0.05 mm/s) with a 4- or 5-mm-diameter brass cylinder equipped with a laser-Doppler probe, combined with ipsilateral common carotid artery occlusion. The microvascular blood flow of PMBSF during compression ischemia was maintained at 18% to 20% of baseline flow for 1 hour. The total infarction volume was measured by 2,3,5-triphenyltetrazolium chloride staining at several reperfusion times, and pathological examination was performed on hematoxylin-eosin–stained sections.

Results—— The infarct volumes were 36.5±9.2 (n=9), 40.7±7.7 (n=7), and 36.6±6.4 mm³ (n=5) at 24 hours, 72 hours, and 7 days after ischemia, respectively, with no significant differences among these values. There was no evidence of damage to white matter or to deep gray matter and no evidence of hemorrhage. The topographic distribution of the damaged tissue was in good agreement with that of PMBSF.

Conclusions—— This stroke model produces a highly consistent cortical infarct in PMBSF and can facilitate the study of behavioral, functional, and structural consequences after cerebral ischemia/reperfusion in the rat somatosensory cortex.

Key Words: cerebral blood flow • cerebral ischemia • neuronal plasticity • stroke, experimental • somatosensory cortex • rats

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