Gibb L, Bishop S P, Kruger F A
Recent Adv Stud Cardiac Struct Metab. 1975;8:333-41.
To determine whether hypoxia per se could initiate myocardial ribonucleic acid (RNA) synthesis, isolated rat hearts were subjected to varying degrees of hypoxic perfusion in a modified Langendorff apparatus. Following a 30-min aerobic stabilization period the hearts were perfused for 30 min with media gassed with mixtures containing O:96% O2, 4% CO2, balance N2. Immediately following the stress period, the hearts were perfused for an additional 30 min with oxygenated media containing radiolabeled uridine, and the incorporation into RNA was determined. Exposure of hearts to 48% O2 resulted in a slight but nonsignificant increase in uridine incorporation. Reduction of perfusate oxygen to 24% caused a significant increase in label incorporation into RNA over that of the aerobic controls. Further reductions in oxygen tension resulted in concomitant increases in uridine incorporation, with the highest levels seen following 30 min of anoxia. Performance was not significantly different from that of controls during the aerobic labeling period. Exposure of hearts to brief (5 min) anoxic perfusion also resulted in significant increases in RNA synthesis during the posthypoxic perfusion period. It is concluded that intermittent hypoxia can initiate the biochemical mechanisms which result in increased myocardial RNA synthesis.
为了确定低氧本身是否能启动心肌核糖核酸(RNA)合成,在改良的Langendorff装置中,对离体大鼠心脏进行不同程度的低氧灌注。在30分钟的有氧稳定期后,心脏用含有96% O₂、4% CO₂、其余为N₂的混合气体吹入的培养基灌注30分钟。应激期结束后,立即用含有放射性标记尿苷的氧合培养基对心脏再灌注30分钟,并测定尿苷掺入RNA的情况。将心脏暴露于48% O₂中,尿苷掺入量略有增加,但无统计学意义。将灌注液中的氧含量降至24%,导致与有氧对照组相比,RNA中标记物的掺入量显著增加。进一步降低氧张力导致尿苷掺入量随之增加,在缺氧30分钟后达到最高水平。在有氧标记期,心脏的功能与对照组无显著差异。将心脏短暂(5分钟)暴露于缺氧灌注中,也会导致低氧后灌注期RNA合成显著增加。结论是间歇性低氧可启动导致心肌RNA合成增加的生化机制。