Induction of reproducible brain infarction by photochemically initiated thrombosis

Authors

  • Dr Brant D. Watson PhD,

    Corresponding author
    1. Cerebral Vascular Discular Researh Center and the Department of Neurology, University of Miami School of Medicine, Miami, FL 31101
    • Department of Neurology (D4-5), University of Miami School of Medicine, P.O. Box 016960, Miami, FL 33101
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  • W. Dalton Dietrich PhD,

    1. Cerebral Vascular Discular Researh Center and the Department of Neurology, University of Miami School of Medicine, Miami, FL 31101
    2. Department of Anatomy and Cell Biology, University of Miami School of Medicine, Miami, FL 31101
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  • Raul Busto BS,

    1. Cerebral Vascular Discular Researh Center and the Department of Neurology, University of Miami School of Medicine, Miami, FL 31101
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  • Mitchell S. Wachtel BS,

    1. Cerebral Vascular Discular Researh Center and the Department of Neurology, University of Miami School of Medicine, Miami, FL 31101
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  • Myron D. Ginsberg MD

    1. Cerebral Vascular Discular Researh Center and the Department of Neurology, University of Miami School of Medicine, Miami, FL 31101
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Abstract

We have used a photochemical reaction in vivo to induce reprodcible thrombosis leading to cerebral infarction in rats. After the intravenous injection of rose bengal, a potent photosensitzing dye, an ischemic lesion was formed by irradiating the left parietal convexity of the exposed skull for 20 minutes with green light(560nm) from a filtered xenon arc lamp. Animals were allowed to surivive form 30 minutes to 15 days after irradiation. Early microscopic alerations within the irradiated zone included the formation of thrombotic plugs and adjacent red blood cell stasis within pial and parenchymal vessels. Scanning electron microscopy revealed frequent platelet aggregates adhering to the vascular endothelium, often resulting in vascular occlusion. Carbon-black brain perfusion demonstrated that occlusion of vascular channels progressed after irradiation and was complete within 4 hours. Histopathological examination at 1, 5, and 15 days revealed that the associated infarct evolved reproducibly through several characteristic stages, including a phase of massive macrophage infiltration. Although cerbral infarction in this model is initiated by thrombosis of small bolld vessels, the fact that the main pathological features of stroke are consistently reproduced should permit its use in assessing treatment regimens, Further, the capability of producing infarction in preselected cortiacal regions may facilitate the study of behavioral, functional, and structural consequences of acute and chronic stroke.

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