间歇性低氧适应的心脏保护

间歇性低氧（intermittent hypoxia,IH）是指一定时间间断地暴露于低氧环境,而其余时间处于常氧环境。IH是机体某种生理和病理状态下的低氧形式。研究表明：间歇性低氧适应（IHadaptation）,类似缺血预适应（ischemic preconditioning,IPC）和长期高原低氧适应（long-termhigh-altitude hypoxic adaptation,LHA）,具有明显的心脏保护作用,表现为增强心肌对缺血／再灌注损伤的耐受性、限制心肌梗死面积和形态学改变、抗细胞凋亡、促进缺血／再灌注心脏舒缩功能的恢复,以及抗心律失常。尽管IH对心脏的保护作用不容质疑,但其作用机制远未阐明。IH心脏保护作用可能涉及氧的运输、能量代谢、神经体液调节、抗氧化酶、应激蛋白、腺苷系统、ATP敏感钾通道、线粒体及其钙调控、一氧化氮和蛋白激酶等多方面机制,并受低氧处理方式、动物年龄和性别等因素影响。IH心脏保护持续时间明显长于IPC,而对机体的不良影响远小于LHA,具有潜在的应用价值。

The cardioprotection of intermittent hypoxic adaptation

Intermittent hypoxia (IH), or periodic hypoxia is referred as exposure to hypoxia interrupted by normoxia that occurs under many physiological and pathophysiological conditions. A lot of researches showed that IH adaptation, like ischemic preconditioning (IPC) and long-term high-altitude hypoxic adaptation (LHA), had significant cardioprotective effects including increasing the tolerance of myocardium to ischemia/reperfusion injury, limiting infarction size and morphologic damage, inhibiting apoptosis of myocardial cells, enhancing recovery of cardiac function in ischemia/reperfusion, and antiarrhythmia. However, the precise mechanisms underlying the protective effects of IH against ischemia/reperfusion injury are far from clear. The potential candidates participating in the protective effects of IH include oxygen transport, energy metabolism, neurohumoral regulation, antioxidase, stress protein, adenosine, ATP-sensitive potassium channel, mitochondrion, calcium control, nitric oxide and protein kinase. The effects of IH are affected by the protocol of hypoxic exposure, age and sex of experimental animals. IH adaptation, for longer lasting time than IPC and lesser side effect than LHA, might have a practical value for using.