间歇性低压低氧对过氧化氢心肌细胞损伤的保护作用

Protective effect of intermittent hypobaric hypoxia on cardiomyocytes injury induced by hydrogen peroxide

目的:观察慢性间歇性低压低氧对过氧化氢所致心肌细胞损伤的保护作用及其机制。方法:雄性豚鼠20只,随机分为两组(n=10):对照组(non-IHH)、低氧组(IHH)。低氧组豚鼠于低压氧舱接受28 d(海拔5 000 m、每天6 h)的低压低氧处理。胶原酶方法急性分离心肌细胞。细胞动缘探测系统测定过氧化氢对各组细胞收缩力的变化。生化方法测定各组丙二醛(MDA)、乳酸脱氢酶(LDH)及超氧化物歧化酶(SOD)和过氧化氢酶(CAT)的变化。结果:①过氧化氢可使心肌细胞出现收缩、舒张紊乱,但IHH处理使其出现的潜伏期明显延长。②给予过氧化氢(300μmol/L,10 min)使来自于non-IHH或IHH的心肌细胞LDH、MDA含量均明显增加,但IHH心肌细胞LDH、MDA含量明显低于non-IHH心肌细胞的LDH、MDA含量。③经IHH处理组的心肌细胞SOD,CAT活性均明显高于non-IHH组。给予过氧化氢使来自于non-IHH或IHH的心肌细胞SOD,CAT活性均明显降低,但IHH心肌细胞SOD,CAT活性明显高于non-IHH心肌细胞的SOD,CAT活性。结论:IHH具有对抗过氧化氢心肌细胞损伤的作用,可能与其增强抗氧化酶活性有关。

Objective： To observe the protective effect and mechnism of intermittent hypobaric hypoxia（IHH） on cardiomyocytes induced by hydrogen dioxide. Methods： Male guinea pigs were divided randomly into two groups （n = 10）： intermittent hypoxia group（IHH）, and control group（non-IHH）. The IHH guinea pigs were exposed to a simulated 5 000 m high altitude and hypoxia in hypobaric chamber for 28 d, 6 h/d. The control guinea pigs were kept in the same environment as IHH except hypoxia exposure. Cardiomyocytes were enzymatically isolat- ed from left ventricle of non-CIHH or CIHH guinea pigs. The contractile was assessed in guinea pigs by a video-based motion edge-detection system. The contents and activities of malondialdehyde（MDA）, lactatdehydrogenase（LDH） and antioxidant enzymes were evaluated by using biochemical methods. Results： QHydrogen peroxide could induce contractile and diastol dysfunction, the latent period was longer in IHH car- diacmyocytes. QAfter hydrogen peroxide（300 t.a＇nol/L, 10 min） perfusion, LDH and MDA contents in supernatant increased significantly in non-IHH and CIHH cardiomyocytes （ P 〈 0.01 ）, Whereas the contents of MDA and LDH in IHH cardiomyocytes were lower than those in non- IHH eardiomyocytes （P 〈 0.01 ）. （~） The activities of superoxide dismutase （SOD） and eatalase （CAT） were significantly increased in the myocardium of IHH guinea pigs, after hydrogen peroxide （300 tanol/L, 10 min） perfusion, SOD and CAT activities decreased significantly in non-IHH and CIHH cardiomyocytes （ P 〈 0.01 ）, whereas the activities of SOD and CAT in CIHH cardiomyocytes were still higher than those in non-IHH cardiomyocytes. Conclusion： IHH had a protective effect on cardiomyocytes injury induced by hydrogen peroxide, which might re- late with its antioxidation effects.