Inhibition of nitric oxide synthase transforms carotid occlusion-mediated benign oligemia into <i>de novo</i> large cerebral infarction.

ABSTRACT: Rationale: It remains unclear why unilateral proximal carotid artery occlusion (UCAO) causes benign oligemia in mice, yet leads to various outcomes (asymptomatic-to-death) in humans. We hypothesized that inhibition of nitric oxide synthase (NOS) both transforms UCAO-mediated oligemia into full infarction and expands pre-existing infarction. Methods: Using 900 mice, we i) investigated stroke-related effects of UCAO with/without intraperitoneal administration of the NOS inhibitor (NOSi) N_ω-nitro-L-arginine methyl ester (L-NAME, 400 mg/kg); ii) examined the rescue effect of the NO-donor, molsidomine (200 mg/kg at 30 minutes); and iii) tested the impact of antiplatelet medications. To corroborate preclinical findings, we conducted clinical studies. Results: UCAO

SUBMITTER: Kim H 

PROVIDER: S-EPMC11671383 | biostudies-literature | 2025

REPOSITORIES: biostudies-literature