Carotid artery occlusion causes reversible brain damage in rat.
In order to assess the density and distribution of brain damage after pure focal ischemia uncomplicated by hypotension or hypoxia, ischemia was produced by occlusion of one and/or both common carotid arteries (CCA) temporarily or permanently in the rat, followed by 3 months recovery. The brains were perfusion-fixed with formaldehyde, embedded in paraffin, subserially sectioned, and stained with hematoxylin-eosin/cresyl violet. Mild ipsilateral neuronal damage was observed after unilateral permanent occlusion, but confined only to the hippocampus. Damage of neocortical neurons began to appear after 1 day following bilateral permanent occlusion. Damage was worst over the superolateral convexity of both hemispheres, CA 4 and subiculur neurons; subsequently other sectors of hippocampus and other brain structures were affected. Some damaged neurons in the superficial cortex and CA 1 sector of hippocampus, and almost all in the other regions of brain reverted to normal profile by 3 months of recovery. All brain structures showed normal profiles, except a relative neuronal rarefication in neocortex and CA 1 sector of hippocampus after 3 months of recovery. These results suggests that only CCA occlusion causes partial/incomplete ischemia in the rat brain, where damaging effects are counterbalanced by metabolic and circulatory adjustments.
Aftabuddin
M
M
Department of Physiology and Pathology, Okayama University School, Japan.
Islam
N
N
Moriwaki
A
A
Hori
Y
Y
D000818:Animals; D001921:Brain / Q000473:pathology* / Q000503:physiopathology; D002545:Brain Ischemia / Q000209:etiology* / Q000473:pathology / Q000503:physiopathology; D017536:Carotid Artery, Common; D016893:Carotid Stenosis / Q000150:complications*; D004569:Electroencephalography; D008297:Male; D051381:Rats; D017208:Rats, Wistar; D013997:Time Factors