短期间歇性低氧暴露对小鼠心肌氧化应激及心脏功能的影响研究

欧伟; 梁羽; 卿羽; 邓艳; 吴畏; 李涛

doi:10.12182/20220160103

短期间歇性低氧暴露对小鼠心肌氧化应激及心脏功能的影响研究

The Effect of Short-Term Intermittent Hypoxia Exposure on Mouse Myocardial Oxidative Stress and Cardiac Function

摘要

摘要:
目的探讨短期间歇性低氧暴露（intermittent hypoxia, IH）对小鼠心肌结构和功能的影响。
方法采用随机分组对照研究的方法，将30只雄性C57BL6/J小鼠随机分为常氧组和低氧（IH）组。IH组采用常压低氧方式，将小鼠暴露于10%浓度氧气中，每天8 h，连续14 d。常氧组小鼠暴露于常压常氧环境，其余操作同IH组。观察暴露期间小鼠生长情况，暴露结束后检测小鼠运动耐量、离体心脏功能、心脏组织学、心肌酶学，以及蛋白脂质过氧化等氧化应激相关指标。
结果两组小鼠运动耐量无明显差异，IH小鼠离体心肌做功能力增加（P<0.05）。与常氧组比较，IH组小鼠心肌电镜表现明显异常，血浆肌酸肌酶同工酶含量升高（P<0.05）；组织活性氧簇水平、蛋白质羰基化水平及丙二醛含量均升高（P<0.05）。
结论 IH暴露诱导小鼠心肌氧化应激损伤，心肌肌纤维结构改变，但不足以损害小鼠的运动耐力和离体心脏的收缩功能。

Abstract:
Objective To investigate the effect of short-term intermittent hypoxia (IH) on the structure and function of mouse myocardium.
Methods Thirty male C57BL6/J mice were randomly assigned to two groups, a control (Con) group and an IH group exposed to hypoxic treatment at atmospheric pressure. The IH group received 10% oxygen pretreatment for 8 hours per day on 14 consecutive days, while the Con group was exposed to normoxia environment and all the other treatment the group received were identical to those given to the IH group, The body mass of the mice was monitored daily during the treatment. The exercise tolerance and the cardiac function of isolated heart were assessed at the end of IH exposure. Additionally, analysis was conducted regarding myocardial enzymology, histology, and other indicators relevant to oxidative stress, including protein carbonylation and lipid peroxidation.
Results There was no significant difference in the exercise tolerance between the two groups. Nevertheless, IH mice showed enhanced cardiac function during isolated heart perfusion (P<0.05). As compared to the control group, prominent alterations of myocardial structure were detected by transmission electron microscopy of the IH heart, accompanied by elevated creatine kinase-MB levels (P<0.05). The levels of myocardial reactive oxygen species, protein carbonylation and lipid peroxidation were all significantly upregulated in the IH group as compared to the control group (P<0.05).
Conclusion IH exposure induced myocardial oxidative stress damage and myofibrillar structural alteration in mice, but did not impair the exercise tolerance of the mice or the contractile function of the isolated heart.

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