Posthypoxia stimulation of ribonucleic acid synthesis in the isolated perfused rat heart.
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.
D000332:Aerobiosis; D000818:Animals; D006321:Heart / Q000503:physiopathology; D006339:Heart Rate; D000860:Hypoxia / Q000378:metabolism*; D008297:Male; D009124:Muscle Proteins / Q000096:biosynthesis; D009206:Myocardium / Q000378:metabolism*; D010477:Perfusion; D011312:Pressure; D012313:RNA / Q000096:biosynthesis*; D051381:Rats; D014529:Uridine / Q000378:metabolism
D009124:Muscle Proteins; D012313:RNA; D014529:Uridine