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Protective effect of target controlled infusion of dexmedetomidine on cerebral ischemia-reperfusion injury and its mechanism

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Author:
No author available
Journal Title:
Chinese Journal of Biomedical Engineering
Issue:
5
DOI:
10.3760/cma.j.cn115668-20210622-00147
Key Word:
急性脑梗死;缺血-再灌注损伤;右美托咪定;分子机制;Acute cerebral infarction;Ischemia reperfusion injury;Dexmedetomidine;Molecular mechanism

Abstract: Objective:To investigate the protective effect of dexmedetomidine against cerebral ischemia-reperfusion (I/R) injury caused by recanalization and its probable molecular mechanism during interventional thrombectomy in patients with acute cerebral infarction (ACI) .Methods:Included in this study were a total of 120 ACI patients who had developed cerebral I/R injury after thrombectomy and were admitted to our hospital between January 2018 and January 2021. The patients were randomized into the control group and study group by random number table. The patients in the control group received routine treatment such as oxygen therapy, dehydration, and antiplatelets. In addition to these, the patients in the study group were given dexmedetomidine using an infusion pump starting from admission to 72 hours after the procedure. After the re-do thrombectomy, the two groups were compared for NIHSS and ADL scores, total treatment response, serum levels of superoxide dismutase (SOD) , malondialdehyde (MDA) , neuron specific enolase (NSE) , S-100B, TNF-α, and IL-6.Results:The NIHSS and ADL scores were improved after thrombectomy in either group. Compared with the control group, the study group receiving perioperative dexmedetomidine showed significantly greater improvement in NIHSS and ADL scores, with statistically difference ( P<0.05) . The study group showed higher response to treatment than did the control group, with statistically significant difference ( P<0.05) . Before the procedure, there were no significant differences in serum levels of SOD, MDA, NSE, S-100B, TNF-α, and IL-6 between the two groups ( P>0.05) . After routine treatment w/o dexmedetomidine, the control group had higher levels of MDA, NSE, S-100B, TNF-α and IL-6, and lower content of SOD in serum, compared with the study group. These differences were statistically significant ( P<0.05) . Conclusion:Perioperative dexmedetomidine can significantly protect patients against cerebral I/R injury, probably via a mechanism related to the anti-oxidative stress and anti-inflammatory effects of dexmedetomidine.

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