Abstract 120: Tissue Kallikrein Attenuates Early Ischemic Edema Progression By Increasing The Glymphatic System Kinetics In Pmcao Mice

Abstract

The glymphatic system (GS) is a perivascular fluid exchange pathway, that is crucial for maintaining brain homeostasis, and may contribute to ischemic edema. Tissue Kallikrein treatment provides cerebral infarction patients with vasodilatory activity, which may facilitate the kinetics in GS. We hypothesized that Tissue Kallikrein could attenuate early ischemic edema following blood interruption by altering the kinetics of the GS. In this study, we evaluated the effects of Tissue Kallikrein on mice acute ischemic edema in pMCAO mice. A fluorescent tracer was injected into the striatum of mice, and the proportion of area infused by the fluorescent tracer in the brain parenchyma was measured to assess the kinetics of the GS. The effect of Tissue Kallikrein on edema was determined by DWI/T2 mismatch, ischemic edema progression was indicated by a mismatch between diffusion-weighted imaging (DWI) and T2-weighted imaging (T2WI), that is, an acute ischemic lesion on DWI without a corresponding lesion on T2WI. Concurrently, correlation analysis was performed for the kinetics and the time windows of DWI/T2 mismatch. Our results indicated that Tissue Kallikrein attenuated brain edema was associated with improved GS kinetics in mice with pMCAO. In brief, this study shows the neuroprotective effects of Tissue Kallikrein in ischemic edema for the first time in pMCAO mice by boosting the GS kinetics.