Posterior communicating artery remodeling in chronic cerebral hypoperfusion

Abstract

Bilateral carotid artery occlusion (BCAO) is an established model of chronic cerebral hypoperfusion that causes vascular cognitive impairment (VCI). To compensate for the occlusion of the carotid arteries, flow from the vertebrobasilar system may increase, and may alter the structure of the posterior communicating artery (PComA). The aim of this study was to understand how BCAO affects the PComA, and we hypothesized that BCAO would cause outward remodeling of the PComA. 20 week old Long Evans rats had BCAO. Data are mean± SEM, SHAM vs BCAO. 5 weeks later the rats had VCI as evidenced by an increased latency to find the platform (7±0.8 vs 28±1.3 s, p<0.05, ANOVA) in Morris water maze testing and a decrease in novel exploration quotient (0.7±0.03 vs 0.5± 0.02, p<0.05, ANOVA) in novel object testing. Structure of PComAs was assessed by pressure myograph (data shown at 80 mmHg). Lumen diameter was increased in BCAO (148±6.1 vs 441±30μm, p<0.05, ANOVA). Wall/lumen ratio was reduced (0.1±0.01 vs 0.04±0.01, p<0.05, ANOVA) while stress was increased (431±32 vs 1106±160 dynes/cm2, p<0.05, ANOVA) in the BCAO. These data suggests that, increased flow through the PComA causes outward remodeling and begets investigation of the reactivity of the PComA. Modulating blood flow through the PComA may be a therapeutic target for VCI.