中文摘要：

目的探讨慢性间歇性低压低氧（CIHH）对发育大鼠心脏的保护作用及其热休克蛋白所起的作用。方法新生♂SD大鼠20只,随机分为两组：CIHH处理组（CIHH）和对照组（CON）。CIHH动物（连同母鼠）接受56 d相当于海拔3 000 m的低压低氧处理（5 h/d）。应用导管法描记左心室功能及血液动力学,包括左室峰压（LVSP）、左室舒张末压（LVEDP）、左室压力最大变化速率（±LVdp/dtmax）、动脉收缩压（SAP）和心率（HR）,并观察急性低氧/复氧对其影响。应用半定量RT-PCR技术检测各组动物心肌热休克蛋白27（HSP27）、热休克蛋白70（HSP70）和热休克蛋白90（HSP90）mRNA的表达。结果①基础状态下,CON组动物与CIHH组动物之间左心室功能和血液动力学无差异（P〉0.05）;急性低氧/复氧导致发育大鼠LVSP、±LVdp/dtmax、SAP降低,HR减慢（P〈0.05）,但CIHH大鼠各参数变化明显小于CON动物（P〈0.05）。②基础状态下,CIHH动物心肌HSP70 mRNA表达明显高于CON动物（P〈0.05）;急性低氧/复氧状态下,CIHH动物心肌HSP27和HSP70 mRNA表达高于CON动物（P〈0.05）。结论 CIHH可通过促进心肌热休克蛋白27和热休克蛋白70表达,增强发育大鼠心肌抗急性低氧/复氧损伤能力。

英文摘要：

Aim To explore the cardiac protection of chronic intermittent hypobaric hypoxia（CIHH）and the role of heat shock protein（HSP）in developing rats.Method Twenty neonatal male Sprague-Dawley rats were divided randomly into two groups：CIHH group and control group.The rats in CIHH group were exposed the hypobaric hypoxia mimicking 3 000 m altitude for 56 days,5 hrs each day.The left ventricular function and hemodynamics including left ventricular systolic pressure（LVSP）,left ventricular end-diastolic pressure（LVEDP）,velocity of left ventricular pressure（±LVdp/dtmax）,systolic arterial blood pressure（SAP）and heart rate（HR）were recorded using catheterization technique.The mRNA of HSP27,HSP70 and HSP90 was measured by semi-quantitative reverse transcription-polymerase chain reaction（RT-PCR）.Results ① There were no differences in the left ventricular function and hemodynemics between CIHH and control groups（P0.05）under basic normoxia condition.During acute hypoxia/reoxygenation,LVSP,±LVdp/dtmax,SAP and HR were decreased（P0.05）in developing rats,but the change in CIHH rats was significantly smaller than that in control rats（P0.05）.② The expression of HSP70 mRNA in CIHH rats was higher than that in control rats（P0.05）under basic normoxia condition.During acute hypoxia/ reoxygenation,the expression of HSP27,and HSP70 mRNA in CIHH animals was higher than that in control animals（P0.05）.Conclusion CIHH can protect heart against acute hypoxia/reoxygenation injury through increasing HSP27 and HSP70 expression in developing rats.