Serum from Stroke Patients with High-Grade Carotid Stenosis Promotes Cyclooxygenase-Dependent Endothelial Dysfunction in Non-ischemic Mice Carotid Arteries

Figures

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  Fig. 1. Effects of ischemic stroke serum on acetylcholine relaxations in male OF-1 mice common carotid arteries. Concentration–response curves to acetylcholine in mice carotid arteries incubated in the absence (no serum) or presence (10%) of ischemic stroke serum (A), healthy control serum (B), or serum from stroke patients that suffered or not from an event (stroke recurrence or vascular death) (C). The results are mean ± SEM for n = 11–26 (no serum), n = 20 (healthy control serum), n = 30 (acute stroke serum), n = 19 (no event), n = 11 (event)

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  Fig. 2. Concentration–response curves to acetylcholine in male OF-1 mice common carotid arteries in the absence (control) or presence (10%) of ischemic stroke serum. Vessels were exposed to serum from ischemic stroke patients (within 7 days poststroke) with low-to-moderate degree (LMGS stroke serum) or high-degree (HGS stroke serum) carotid stenosis (A) and with HGS stroke serum from the same patients obtained within 7 days or at 1-year poststroke (B). The results are mean ± SEM of (A) n = 26 (control), 20 (LMGS stroke serum), 10 (HGS stroke serum), and of (B) n = 6 (HGS stroke serum 7 days) and n = 6 (HGS stroke serum 1 year)

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  Fig. 3. Concentration–response curves to acetylcholine in male OF-1 mice common carotid arteries incubated in the absence (control) or presence (10%) of high-grade stenosis (HGS) stroke serum. Vessels were treated with the nonselective NO synthase inhibitor, L-NAME (300 µM) (A), or the nonselective COX inhibitor, indomethacin (indo, 10 µM) (B). The results are mean ± SEM of n = 6 (A) and n = 5 (B) per group

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  Fig. 4. Concentration–response curves to acetylcholine in male OF-1 mice common carotid arteries in the absence (control) or presence (10%) of high-grade stenosis (HGS) stroke serum. Vessels were treated with the selective COX-1 inhibitor, SC-560 (0.3 µM) (A), or the selective COX-2 inhibitor, NS-398 (1 µM) (B). Data are presented as mean ± SEM of n = 5 (A and B) per group

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  Fig. 5. Concentration of circulating inflammatory molecules in healthy control plasma and in plasma from patients with high-grade stenosis (HGS stroke plasma) obtained within 7 days or at 1-year poststroke. The levels of IL-1β (A), IL-6 (B), TNF-α (C), sICAM-1 (D), sVCAM-1 (E), and fractalkine (F) are shown. Data highlighted in green squares indicate samples from the same patients. Data are presented as mean ± SEM of n = 20 (healthy control plasma), n = 10 (HGS stroke plasma 7 days), and n = 5 (HGS stroke plasma 1 year); *P < 0.05 vs. Healthy control plasma by one-way ANOVA with Tukey’s post hoc test; #P < 0.05 one-way ANOVA