CLINICAL studies of patients with stenosis and occlusion of the internal carotid artery1 have stimulated studies of the pathogenesis of cerebral infarction. Observations of experimental ischemic lesions of the brain by light microscopy, with reference to small vessels, were reported by Meyer.2 His findings confirmed the predictions of earlier studies that infarction was the result of ischemic anoxia producing damage to both neural and vascular tissues in the supply of the occluded vessel. The earliest descriptions of cerebral lesions by electron microscopy were by Schultz and Pease3 who studied cicatrix formation after sterile wounds of rat cortex; however, there was little description of the vascular bed in healed lesions. Hills4 described ultrastructural changes in the capillary bed of rat cerebral cortex up to four days after anoxic-ischemic encephalopathy with no discrete areas of infarction. Other experimental lesions induced by local cold injury,5,6 hydration of the
CALHOUN CL, MOTTAZ JH. Capillary Bed of the Rat Cerebral Cortex: The Fine Structure in Experimental Cerebral Infarction. Arch Neurol. 1966;15(3):320–328. doi:10.1001/archneur.1966.00470150098015
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