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  • Title: Effect of blood pressure on early neurological deterioration of acute ischemic stroke patients with intravenous rt-PA thrombolysis may be mediated through oxidative stress induced blood-brain barrier disruption and AQP4 upregulation.
    Author: He Y, Yang Q, Liu H, Jiang L, Liu Q, Lian W, Huang J.
    Journal: J Stroke Cerebrovasc Dis; 2020 Aug; 29(8):104997. PubMed ID: 32689627.
    Abstract:
    OBJECTIVE: To study association between blood pressure (BP) and development of early neurological deterioration (END) in acute ischemic stroke patients with intravenous rt-PA thrombolysis and its possible mechanism. METHODS: We prospectively collected data of acute ischemic stroke patients with intravenous rt-PA thrombolysis from March 2015 to June 2019. The collected data include general, clinical data and laboratory test. Moreover, serum levels or activity of malondialdehyde (MDA), superoxide dismutase (SOD), matrix metalloproteinase-9 (MMP-9), occludin(OCLN), ZO-1 and aquaporin 4(AQP-4) were determined. RESULTS: A total of 357 acute ischemic stroke patients received intravenous rt-PA thrombolysis and 16 cases were eventually excluded. Finally, 341 patients were eligible in this study and 65 patients (19.06%) experienced END. Mean systolic blood pressure (SBP) within 24 h, serum levels or activity of MDA, SOD, MMP-9, ZO-1, OCLN, AQP-4 at 24 h after thrombolysis were the independent predictors for END in the total and hypertension population using multivariate logistic regression analysis, and mean SBP within 24 h was the best predictor for END. Receiver operating characteristic (ROC) analysis found that cutoff mean SBP for END was 148.16 mmHg, and sensitivity was 85.6%. The best target SBP level is 140ཞ149 mmHg. Further, spearman correlation tests indicated that BP levels were directly proportional to serum levels or activity of MDA, MMP-9, ZO-1, OCLN, AQP-4 at 24 h after thrombolysis and neurological deterioration severity. CONCLUSIONS: END frequently occurs after thrombolysis, and the best predictor of END is SBP which may be mediated through oxidative stress induced blood-brain barrier disruption and AQP4 upregulation.
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