Chronic cerebral hypoperfusion protects against acute focal ischemia, improves motor function, and results in vascular remodeling.

Atherosclerosis may cause severe stenosis of the arteries supplying the brain, which induces chronic cerebral hypoperfusion. Although an infarction often occurs in this area, it is uncertain how brain vessels respond to the chronic hypoperfusion or how the vascular responses are related to stroke severity when the area has been subjected to severe ischemia. To address these uncertainties, we induced chronic cerebral hypoperfusion in Sprague-Dawley rats with a bilateral common carotid artery ligation (BCAL). A middle cerebral artery occlusion/reperfusion (MCAO/R) was introduced with a nylon suture four weeks after either BCAL (BCAL-MCAO) or a sham operation (Sham-MCAO). Motor disability scores and infarct sizes, based on 2,3,5-triphenyltetrazolium chloride staining, were significantly reduced with BCAL-MCAO treatment compared with sham-MCAO treatment (P<0.01). The diameters of the posterior cerebral, posterior communicating, and basilar arteries on the brain surface were larger and more tortuous in BCAL-treated rats (P<0.01). The density of large capillary- and arteriole-sized vessels in the brain parenchyma also increased in BCAL-treated rats (P<0.05). Strokes were less severe when the vicinity subjected to infarction was preconditioned with chronic cerebral hypoperfusion. Increasing the vascular reserve with adaptive vascular remodeling may have contributed to this response.