低氧及常氧灌流对离体大鼠心脏应激蛋白的诱导

目的和方法：观察低氧灌流和常氧灌流诱导离体大鼠心脏的应激蛋白合成。结果：低氧和常氧灌流均可诱导３个分子量为７０ｋＤａ的一组应激蛋白（ｓｐ６８，７０和７２）合成显著增加，５个分子量为６０ｋＤａ的一组应激蛋白（ｓｐ５４－６５）合成也有所增加。比较不同灌流方式和时程对应激蛋白合成的影响，发现７０ｋＤａ的一组应激蛋白合成量在常氧灌流的离体心脏中高于低氧灌流；并且该组应激蛋白合成量在经两种灌流方式处理１ｈ的以脏高于灌流处理２ｈ的心脏。结论：应激蛋白合成量并不与应激原的迭加或与细胞受环境损害的严重性成正比。对灌流的离体心脏而言，缺血可能是诱导应激蛋白合成的主要因素，低氧及常氧则起调节合成量的作用

Induction of stress proteins in hypoxic and normoxic perfused isolated rat hearts

AIM and METHODS:Inducton of stress proteins was observed in isolated rat hearts by hypoxic and normoxic perfusions. RESULTS:The three 70kDa stress protein isoforms (SP 68,70 AND 72)were distinctly increased in the right and left myocardiums in both perfused isolated hearts. Moreover,five 60 kDa stress protein isoforms were also found to be increased compared with the controls. To determine the effect olf different perfusion ways and periods on synthesis of the stress proteins,it was demonstrated that the amount of SP70 isoforms synthesized in the normoxic perfused isolated hearts was higher than that in the hypoxic perfused isolated hearts,and the enhanced amount of these proteins in the isolated hearts treated with hypoxic and normoxic perfusions for 1h was more than that for 2h. CONCLUSION:Amount of the stress proteins synthesized was not proportional to the stressors added togather olr the degree of cells damaged. As far as perfused isolatd hearts were concerned,the ischemia stress was most likely a dominator for inducing synthesis of the stress proteins, but the conditions of hypoxia and normoxia were only to regulate the amount of stress proteins synthesized.