中文摘要：

目的观察慢性间歇性低压低氧（chronic intermittent hypobaric hypoxia，CIHH）处理对发育大鼠HSP27、HSP70和HSP90蛋白表达的影响，探讨心肌热休克蛋白在发育大鼠CIHH心脏保护中的作用。方法新生雄性Sprague—Dawley（SD）大鼠20只，随机分为2组，CIHH处理组（CIHH）和对照组（CON）。CIHH发育大鼠（连同母鼠）置于低压氧舱中，接受56d相当于海拔3000m的低压低氧处理（5h／d）。股动脉插管记录动脉血压，左心室插管描记左心室功能，包括左室峰压（left ventrieular systolic pressure，LVSP）、左室压力最大变化速率（left ventricular pressure，±LVdp／dtmax）。应用Western blot技术定量分析各组发育大鼠心肌热休克蛋白27（heat shock protein 27，HSP27）、热休克蛋白70（heat shock protein 70，HSP70）和热休克蛋白90（heat shock protein 90，HSP90）表达。并观察急性低氧／复氧对左心室功能、动脉血压和热休克蛋白（heat shock protein，HSPs）表达的影响。结果基础状态下，CIHH组与CON组发育大鼠的LVSP、±LVdp／dtmax及平均动脉压（mean artery blood pressure，MABP）差异无统计学意义（P〉0．05），但CIHH组发育大鼠心肌HSP27、HSP70和HSP90蛋白表达显著高于CON组发育大鼠；急性低氧／复氧导致发育大鼠LVSP、±LVdp／dtmax及MABP降低，表达增加，而CIHH组发育大鼠心功能参数及MABP降低幅度明显小于CON组发育大鼠，且3种HSPs蛋白表达明显高于CON组发育大鼠（P〈0．05）。结论CIHH可通过增强发育大鼠心肌HSPs蛋白表达发挥心脏保护作用。

英文摘要：

Objective To investigate the effect of chronic intermittent hypobaric hypoxia （CIHH） on the expression of heat shoek protein. （HSPs） 27, HSP70 and HSP90 proteins and the role of HSPs in cardiac protection of CIHH in developing rats. Methods Twenty neonatal male Sprague - Dawley rats were randomly divided into two groups： CIHH treatment group （CIHH）and control group （CON）. The neonatal rats （with maternal rats）in CIHH group were placed in a hypobaric ehamber to get a CIHH mimicking 3 000m high - altitude hypoxia for 56 days, 5 h each day. The catheterization technique was used to record the left ventrieular function and hemodynamics including left ventricular systolic pressure （ LVSP）, velocity of left ventricular pressure （ ± LVdp/dtmax） and mean artery blood pressure （MABP）. Western blot method was used to measure the expression of myocardium HSP27, HSP70 and HSP90. The cardiac heart function, artery blood pressure and HSP expression were recorded under normoxic condition, acute hypoxia and reoxygenation, respectively. Results There were no differences of the left ventricular function and MABP between CIHH and control rats under basic normoxia condition （ P 〉 0.05 ）, but the expression of HSP27, HSP70 and HSP90 in CIHH rats was higher than that in control rats （ P 〈 0.05 ）. During acute hypoxia/reoxygenation, LVSP, ±LVdp/dtmax and MABP were decreased （P 〈 0.05 ） in developing rats, but the change in CIHH rats was remarkably smaller than that in control rats （P 〈 0.05 ）. The expression of HSP27, HSP70 and HSP90 proteins in CIHH group were higher than that in control group （ P 〈 0.05 ）. Conclusion CIHH can protect the heart against acute hypoxia injury through increasing the expression of HSPs proteins in developing rats.