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目的:定量检测暴露于间歇性低氧不同时程后心肌热休克蛋白(HSP70)表达量并探讨HSP70与大鼠心脏对缺血再灌注损伤的耐受性之间的关系。方法:结扎冠脉左前降支造成心肌缺血及再灌注模型;并以逆转录PCR方法检测大鼠心肌HSP70 mRNA的表达量。结果:间歇性低氧暴露14,28,42天后HSP70表达量分别增加2.6,3.6,3.8倍;低氧训练28天后大鼠心脏对缺血-再灌注损伤的耐受性明显增加,缺血和再灌注心律失常诱发评分(AS)显著降低;大鼠脱离低氧环境后,上述作用能够维持2周。而且HSP70的表达量与心肌耐受性的增加存在明显相关(r=0.98,0.92;P<0.01)。结论:间歇性低氧暴露后心肌对缺血-再灌注损伤耐受性的增加与HSP70的表达量有关。
OBJECTIVE: To quantitatively detect the expression of heat shock protein (HSP70) after exposure to intermittent hypoxia at different time points and to explore the relationship between HSP70 and the tolerance of rat heart to ischemia-reperfusion injury. Methods: Ligation of left anterior descending coronary artery caused myocardial ischemia and reperfusion model. The expression of HSP70 mRNA in myocardium was detected by reverse transcription polymerase chain reaction. Results: The HSP70 expression increased by 2.6, 3.6 and 3.8 times respectively after exposed to intermittent hypoxia for 14, 28 and 42 days. The tolerance to ischemia-reperfusion injury was significantly increased after 28 days hypoxia training in rats, Reperfusion arrhythmia induced score (AS) decreased significantly; rats from hypoxic environment, the above effect can be maintained for 2 weeks. Moreover, there was a significant correlation between the expression of HSP70 and myocardial tolerance (r = 0.98,0.92; P <0.01). Conclusion: The increase of myocardial tolerance to ischemia-reperfusion injury after intermittent hypoxic exposure is related to the expression of HSP70.