糖尿病心肌缺血调节作用受损机制及其临床治疗

Impaired mechanism of diabetic myocardial ischemia regulation and its clinical treatment

缺血再灌注损伤(IRI)以缺血缺氧、随后血流恢复为特征,引起组织器官的不可逆转的损伤。缺血再灌注损伤的发病机制复杂,且多方面因素参与,互相关联。现已有大量研究重点关注通过缺血调节方法,提高器官对缺血再灌注损伤的耐受性。糖尿病通过扰乱细胞内信号转导通路,改变心肌细胞对缺血调节方式的应答,增加了心肌细胞对缺血再灌注损伤的易感性。本文旨在归纳糖尿病状态下心肌缺血调节作用受损的可能机制及其临床保护措施。

Ischemia-reperfusion injury（IRI） is characterized by ischemia and hypoxia, followed by blood flow recovery, causing irreversible damage of tissues and organs. The pathogenesis of ischemia-reperfusion injury is complex,and many interrelating factors involved. A large number of studies have focused on improving the tolerance of organs to ischemia-reperfusion injury through ischemic regulation. Diabetes mellitus increases the susceptibility to myocardial ischemia and reperfusion injury by disturbing intracellular signal transduction pathways and alters the response of cardiomyocytes to ischemic regulation. The aim of this study is to summarize the possible mechanisms of myocardial ischemic regulation in diabetic patients and its clinical protective measures.