Abstract Objectives: This study explored the association between insomnia and the clinical outcome of large vessel occlusion Acute Ischemic Stroke (AIS) and attempted to explore its potential mechanisms from the perspectives of inflammation and oxidative stress. Methods: AIS patients who underwent endovascular treatment for large vessel occlusion at Binzhou Central Hospital from 2018 to 2022 (n = 508) were included. Patients were divided into an insomnia group and a non-insomnia group. Insomnia was judged by self-reported Athens Insomnia Scale score. Regression analysis was used to compare the differences in the 24-hour and 7-day National Institutes of Health Stroke Scale (NIHSS) score, Early Neurological Deterioration (END), early adverse event incidence, 90-day prognosis and mortality, and serum bio-markers levels. Results: The incidence of insomnia in the study population was 39.6% (n = 144, insomnia group; n = 364, non-insomnia group). Compared with the non-insomnia group, a worse prognosis outcome (63% vs. 49%, adjusted rate ratio: 1.8, 95% Confidence Interval: 1.2–3.7; p = 0.016), higher 24-h and 7-day NIHSS score (17 [9–36] vs. 13 [5–20]; p = 0.024, and 11 [4‒24) vs. 8 [2‒14]; p = 0.031, respectively), higher END (24% vs. 15%, p = 0.022), and higher incidence of adverse events were observed in the insomnia group (79% vs. 59%, p = 0.010). The 90-day mortality was higher in the insomnia group than that in the non-insomnia group (22% vs. 17%), however, such a difference was not statistically significant. Conclusion: Insomnia is closely related to the clinical outcome of AIS with large vessel occlusion, and inflammation and oxidative stress mechanisms may be involved. Objectives (AIS Methods 201 202 508 included noninsomnia non selfreported self reported 24hour hour 24 7day day 7 (NIHSS END, , (END) 90day 90 biomarkers bio markers levels Results 396 39 6 39.6 144 364 . group) 63% 63 (63 vs 49 49% ratio 18 1 1.8 95 Interval 1.2–3.7 1237 2 3 0.016, 0016 0.016 0 016 0.016) 24h h 17 (1 9–36 936 9 36 [9–36 5–20 520 5 20 [5–20] 0024 024 0.024 4‒24 424 4 [4‒24 2‒14 214 14 [2‒14] 0031 031 0.031 respectively, respectively respectively) 24% (24 15 15% 0.022, 0022 0.022 022 0.022) 79% 79 (79 59 59% 0.010. 0010 0.010 010 0.010) 22% 22 (22 17%, 17% 17%) however significant Conclusion involved 50 (END 39. (6 1. 1.2–3. 123 001 0.01 01 ( 9–3 93 [9–3 5–2 52 [5–20 002 02 0.02 4‒2 42 [4‒2 2‒1 21 [2‒14 003 03 0.03 (2 (7 1.2–3 12 00 0.0 9– [9– 5– [5–2 4‒ [4‒ 2‒ [2‒1 1.2– 0. [9 [5– [4 [2‒ 1.2 [ [5 [2

Abstract Purpose: To investigate the effect of alprostadil on myocardial ischemia/reperfusion (I/R) in rats. Methods: Rats were subjected to myocardial ischemia for 30 min followed by 24h reperfusion. Alprostadil (4 or 8 μg/kg) was intravenously administered at the time of reperfusion and myocardial infarct size, levels of troponin T, and the activity of creatine kinase-MB (CK-MB) and lactate dehydrogenase (LDH) in the serum were measured. Antioxidative parameters, nitric oxide (NO) content and phosphorylated endothelial nitric oxide synthase 3 (p-eNOS) expression in the left ventricles were also measured. Histopathological examinations of the left ventricles were also performed. Results: Alprostadil treatment significantly reduced myocardial infarct size, serum troponin T levels, and CK-MB and LDH activity (P<0.05). Furthermore, treatment with alprostadil significantly decreased malondialdehyde (MDA) content (P<0.05) and markedly reduced myonecrosis, edema and infiltration of inflammatory cells. Superoxide dismutase and catalase activities (P<0.05), NO level (P<0.01) and p-eNOS (P<0.05) were significantly increased in rats treated with alprostadil compared with control rats. Conclusion: These results indicate that alprostadil protects against myocardial I/R injury and that these protective effects are achieved, at least in part, via the promotion of antioxidant activity and activation of eNOS.