Department of Anesthesiology, The Third Affiliated Hospital of Qiqihar Medical College, Qiqihar 161000, China.
J Healthc Eng. 2021 Nov 24;2021:4293900. doi: 10.1155/2021/4293900. eCollection 2021.
This study aimed to explore the effect and mechanism of lidocaine pretreatment combined with dexmedetomidine on oxidative stress in patients with intracranial aneurysm clipping. Many studies have used various drugs such as lidocaine to explore the effect and mechanism of lidocaine pretreatment. A total of 80 patients with intracranial aneurysm clipping surgery were randomly divided into 4 groups: the single lidocaine group, single dexmedetomidine group, lidocaine combined with dexmedetomidine group, and control group. The thread embolism method was used to establish a stable intracranial aneurysm model of Hashimoto rats. Fifty adult rats were randomly divided into a sham operation group, ligation of the left common carotid artery and bilateral posterior branch of renal artery, lidocaine group, dexmedetomidine group, and lidocaine combined with dexmedetomidine group. The colorimetric method was used to determine the oxidative stress indicators in brain tissue: MDA content, SOD activity, and T-AOC content. The western blot method characterized the protein levels related to oxidative stress: nNOS, iNOS, and NADPH oxidase subunits p22phox, gp91phox, and p47phox. The differences in each index between the groups were statistically significant ( < 0.05). Animal experiment results revealed that the content of MDA in the brain tissue of rats in the LD group was significantly lower than that in the single-drug group and sham group. The T-AOC and SOD concentrations in the LD group were significantly higher than those in the single-drug group and sham group, and the differences between the groups were statistically significant ( < 0.05). The protein expression of the LD group was significantly lower than that of the drug-alone group and model group, and the difference between groups was statistically significant ( < 0.05). To sum up, lidocaine pretreatment combined with dexmedetomidine can effectively maintain the hemodynamic stability of patients with intracranial aneurysm clipping and reduce postoperative oxidative stress response. Its mechanism of action may be related to the inhibition of oxidative stress damage mediated by nNOS, iNOS, and p22phox, gp91phox, and p47phox in the hippocampus. Our study has significant and applicable medical aspects in lidocaine pretreatment combined with dexmedetomidine on oxidative stress in patients.
本研究旨在探讨利多卡因预处理联合右美托咪定对颅内动脉瘤夹闭术患者氧化应激的影响及机制。许多研究采用利多卡因等各种药物，探讨利多卡因预处理的作用及机制。将 80 例行颅内动脉瘤夹闭术患者随机分为 4 组：单利多卡因组、单右美托咪定组、利多卡因联合右美托咪定组和对照组。采用线栓法建立稳定的 Hashimoto 大鼠颅内动脉瘤模型。将 50 只成年大鼠随机分为假手术组、结扎左侧颈总动脉及双侧肾动脉后支、利多卡因组、右美托咪定组和利多卡因联合右美托咪定组。采用比色法测定脑组织氧化应激指标：丙二醛（MDA）含量、超氧化物歧化酶（SOD）活性和总抗氧化能力（T-AOC）含量。Western blot 法检测与氧化应激相关的蛋白水平：nNOS、iNOS 及 NADPH 氧化酶亚基 p22phox、gp91phox、p47phox。各组间各指标差异均有统计学意义（ < 0.05）。动物实验结果显示，LD 组大鼠脑组织中 MDA 含量明显低于单药组和假手术组。LD 组 T-AOC 和 SOD 浓度明显高于单药组和假手术组，组间差异有统计学意义（ < 0.05）。LD 组蛋白表达明显低于单药组和模型组，组间差异有统计学意义（ < 0.05）。综上所述，利多卡因预处理联合右美托咪定可有效维持颅内动脉瘤夹闭术患者的血流动力学稳定，降低术后氧化应激反应。其作用机制可能与抑制海马区 nNOS、iNOS 及 p22phox、gp91phox、p47phox 介导的氧化应激损伤有关。本研究在利多卡因预处理联合右美托咪定对颅内动脉瘤夹闭术患者氧化应激的影响方面具有重要的、适用的医学意义。
