%0 Journal Article %T 利多卡因影响心肌缺血再灌注损伤相关机制的研究进展
Research Progress on the Mechanism of Lidocaine Affecting Myocardial Ischemia-Reperfusion Injury %A 吴明潇 %A 杨雪儿 %A 刘博宇 %A 张鑫悦 %A 金莲锦 %A 李罡 %A 温立勇 %A 胡春阳 %J Advances in Clinical Medicine %P 188-195 %@ 2161-8720 %D 2024 %I Hans Publishing %R 10.12677/acm.2024.1461762 %X 心肌缺血再灌注损伤是指供应心肌组织的血流被阻断后,恢复血流再灌注时可能会发生损伤加重的情况,这是一个动态发展的过程,其中包括MIRI相关炎症反应、中性粒细胞的激活和血管内皮功能损伤。心肌缺血会引起炎症反应、氧化应激、免疫紊乱、心肌超微结构变化等一系列损伤性变化,严重的心肌缺血的患者常因发生心律失常而猝死。利多卡因作为对钠通道有阻滞作用的氨基酰胺类中效局部麻醉药,临床上常用于治疗室性心律失常。利多卡因可以减轻机体受伤部位的炎性反应,减少中性粒细胞和巨噬细胞等细胞的聚集,可能通过调节体内炎症因子、中性粒细胞、内皮细胞等心肌损伤相关因素而改变损伤进展。本文就利多卡因可能影响心肌缺血再灌注损伤的相关机制研究进展展开综述。
Myocardial ischemia-reperfusion injury is a condition in which the blood flow supplying myocardial tissue is blocked, and then the injury may be aggravated when the blood flow reperfusion is restored, which is a dynamic developmental process that includes MIRI-related inflammatory response, activation of neutrophils and impairment of vascular endothelial function. Myocardial ischemia causes a series of damaging changes such as inflammatory response, oxidative stress, immune disorders, and ultrastructural changes in the myocardium, and patients with severe myocardial ischemia often die suddenly due to the occurrence of arrhythmias. Lidocaine, as a medium-acting local anesthetic of the aminamide class with a blocking effect on sodium channels, is commonly used clinically for the treatment of ventricular arrhythmias. Lidocaine reduces the inflammatory response at the site of injury, decreases the aggregation of cells such as neutrophils and macrophages, and may alter the progression of injury by modulating myocardial injury-related factors such as inflammatory factors, neutrophils, and endothelial cells in vivo. In this paper, we review the progress of research on the mechanisms related to the possible influence of lidocaine on myocardial ischemia-reperfusion injury. %K 利多卡因,心肌缺血再灌注损伤,炎症因子
Lidocaine %K Myocardial Ischemia-Reperfusion Injury %K Inflammatory Factors %U http://www.hanspub.org/journal/PaperInformation.aspx?PaperID=88872