缺氧对肉鸡心肌细胞内游离Ca2+浓度的影响

 【目的】检测缺氧对肉鸡心肌细胞内Ca2+浓度的影响，阐明缺氧对心肌细胞影响的机制。【方法】利用体外细胞培养技术，以Fluo-3/AM为Ca2+指示剂，用LSCM检测缺氧对体外培养的肉鸡心肌细胞内游离Ca2+浓度的影响。【结果】与常氧组比较缺氧显著引起心肌细胞内游离Ca2+升高（常氧99.3±13.1；缺氧129.4±24.3,P<0.01）,钙通道拮抗剂Verapamil（Ver）和Nifedipine（Nif）可显著抑制缺氧引起的游离Ca2+升高（缺氧＋Ver 100.9±28.2,缺氧＋Nif 107.6±27.7）。【结论】缺氧能够增强心肌细胞的游离Ca2+跨膜转运导致细胞内Ca2+浓度升高，Ca2+通道拮抗剂能够减弱缺氧引起的心肌细胞膜上Ca2+的跨膜转运。

Effect of Hypoxia on the Ca2+ Concentration in Broiler''s Cardiac Muscle Cell

The purpose of this experiment was to study the effect of hypoxia on the Ca2+ concentration in broiler’s Cardiac Muscle Cell (CMC) . The concentration of Ca2+ in the CMC was observed by laser scanning confocal microscope (LSCM). The results showed that hypoxia could significantly increase intracellular Ca2+ of CMC (CMC: normal oxgen:99.3±13.1, hypoxia:129.4±24.3,p<0.01.). The Ca2+ antagonist (nifedipine, Nif; verapamil, Ver) can significantly restrain the Ca2+ influx across the cell membrane of CMC treated by hypoxia (CMC: hypoxia + Ver:100.9±28.2, hypoxia＋Nif:107.6±27.7, p<0.01). Hypoxia is the important cause of ascites syndrome（AS）, myocardial hypertrophy is the typical pathological change .The results suggest that the transmembrane movement of Ca2+ in the CMC maybe play an important role in the development of AS .