右美托咪定调节心肌缺血再灌注损伤相关通路的研究进展

Research progress of dexmedetomidine in regulating pathways related to myocardial ischemia reperfusion injury

急性心肌梗死(AMI)是导致人类死亡的主要原因之一,心肌梗死后的再通导致心肌损伤进一步加重,因此早期的治疗和及时有效的干预措施,对减少AMI患者的总病死率起着重要意义。药物预处理或后处理被证实能够减轻再灌注所带来的损伤,其机制是使相关信号通路激活,控制下游信号蛋白级联反应的发生,从而发挥心脏保护作用。研究发现右美托咪定可以减轻心肌缺血再灌注所造成的损伤。本文现就右美托咪定对心肌保护作用的机制,并讨论可能参与心肌缺血再灌注损伤的信号通路及相关治疗进行综述。

Acute myocardial infarction(AMI) is one of the main causes of human death, and reperfusion after AMI leads to further aggravation of myocardial damage. Therefore, early treatment and timely and effective intervention measures play an important role in reducing the overall mortality of patients with AMI. Pretreatment or post-treatment of drugs has been proved to reduce the injury caused by reperfusion. Its mechanism is to activate related signal pathways and control the occurrence of cascade reaction of downstream signaling proteins, so as to play a protective role in the heart. It is found that dexmedetomidine can alleviate the injury caused by myocardial ischemia reperfusion. In this paper, the mechanism of dexmedetomidine on myocardial protection is reviewed, and the possible signal pathways involved in myocardial ischemia reperfusion injury and related treatments are discussed.