| Objective: A lot of researches showed that chronic intermittent hypobaric hypoxia (CIHH) had significant protective effect on adult rat heart, enhancing the resistance of heart against ischemia/reperfusion or acute hypoxia/re- oxygenation injury, relieving the cardiac function decrease induced by ischemia/reperfusion and anti-arrhythmia. There were many differences on structure and function between adult and developing rat heart. The investigation on effect of CIHH in developing heart, however, was very limited. Furthermore, there was no report on effect of CIHH on expression of heat shock proteins (HSPs) in developing rat heart. The aim of the present study was to explore the protective effect of CIHH against acute hypoxia/reoxygenation injury and the underlying mechanism of HSPs in developing rat heart through the functional and molecular biological methods.Method: Sixty neonatal male Sprague-Dawley rats were divided randomly into six groups: CIHH 28-day treatment group (CIHH28), CIHH 42-day treatment group (CIHH42), CIHH 56-day treatment group (CIHH56), control 28-day group (Con28), control 42-day group (Con42) and control 56-day group (Con56). CIHH animals were put into a hypobaric chamber to get 28 days, 42 days and 56 days CIHH mimicking 3000m altitude (PB = 525 mmHg, PO2 = 108.8 mmHg), 5 hrs/day, respectively. The control animals were kept in the same environment as CIHH rats with free access to water and food except hypoxic exposure. Catheterization was used to trace arterial blood pressure (BP), heart rate (HR), left ventricular systolic pressure (LVSP), left ventricular end-diastolic pressure (LVEDP) and left ventricular velocity of tension development (±LVdp/dtmax) under basic normoxia condition and during acute hypoxia/reoxygenation condition. The mRNA and proteins expression of HSP27, HSP70 and HSP90 were detected by semi-quantitative reverse transcription-polymerase chain reaction (RT-PCR) and Western-blotting, respectively.Results: 1. There were no differences of the left ventricular function among three Con groups (P>0.05) under basic normoxia condition, except that the HR in Con28 was faster than that in Con42 and Con56 (P<0.05). The LVSP and +LVdp/dtmax in CIHH28 were higher than that in CIHH42 and CIHH56 (P<0.05). Also, the LVSP in CIHH28 was higher than that in Con28. During acute hypoxia/reoxygenation, BP, HR, LVSP,±LVdp/dtmax decreased with LVEDP increased (P<0.05), but the changes of dynamics in CIHH rats were smaller than those in Con rats (P<0.05).2. There were no differences of expression in HSPs mRNA between the six groups (P>0.05) under basic normoxia condition. During acute hypoxia/reoxygenation, the expression of HSP90 mRNA was significantly increased (P<0.05) in Con animals. The expression of HSP27, HSP70 and HSP90 mRNA in CIHH rats were significantly increased (P<0.05), especially HSP70 and HSP90 mRNA in CIHH28 rats (P<0.05). The expression of HSPs mRNA was significantly increased in CIHH animals compared with Con animals (P<0.05).3. Protein expression of HSP27 in Con28 rats was higher than that in Con42 and Con56 rats (P<0.01) under basic normoxia condition. Protein expression of HSP27, HSP70 and HSP90 was increased in CIHH rats (P<0.05-0.01) and the increase was the highest in CIHH28 rats under basic normoxia condition. Protein expression of HSPs was increased in all rats during acute hypoxia/reoxygenation, but the increasing of HSPs expression was more significant in CIHH rats than Con rats (P<0.05). The protein expression of HSPs in CIHH28 rats was the highest among CIHH rats.Conclusion: CIHH can protect developing rat heart against acute hypoxia/reoxygenation injury through increasing expression of HSPs mRNA and proteins. |
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