• Mariana Gomez-Smith, Rafal Janik, Conner Adams, Evelyn M Lake, Lynsie A M Thomason, Matthew S Jeffers, Bojana Stefanovic, and Dale Corbett.
• Department of Cellular and Molecular Medicine, Roger Guindon Hall, University of Ottawa, 451 Smyth Road, Ottawa, Ontario K1H 8M5, Canada; Canadian Partnership for Stroke Recovery, 600 Peter Morand Cres., Suite 206 Ottawa, Ontario K1G 5Z3, Canada.
• Neuroscience. 2018 Feb 10; 371: 166-177.

AbstractTo better understand the effects of a diet high in fat, sugar, and sodium on cerebrovascular function, Sprague Dawley rats were chronically exposed to a Cafeteria diet. Resting cerebral perfusion and cerebrovascular reactivity was quantified using continuous arterial spin labeling (CASL) magnetic resonance imaging (MRI). In addition, structural changes to the cerebrovasculature and susceptibility to ischemic lesion were examined. Compared to control animals fed standard chow (SD), Cafeteria diet (CAF) rats exhibited increased resting brain perfusion in the hippocampus and reduced cerebrovascular reactivity in response to 10% inspired CO2 challenges in both the hippocampus and the neocortex. CAF rats switched to chow for one month (SWT) exhibited improved resting perfusion in the hippocampus as well as improved cerebrovascular reactivity in the neocortex. However, the diet switch did not correct cerebrovascular reactivity in the hippocampus. These changes were not accompanied by alterations in the structural integrity of the cerebral microvasculature, examined using rat endothelial cell antigen-1 (RECA-1) and immunoglobulin G (IgG) immunostaining. Also, the extent of tissue damage induced by endothelin-1 injection into sensorimotor cortex was not affected by the Cafeteria diet. These results demonstrate that short-term consumption of an ultra-processed diet reduces cerebrovascular reactivity. This effect persists after dietary normalization despite recovery of peripheral symptomatology.Copyright © 2017 IBRO. Published by Elsevier Ltd. All rights reserved.

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