Lishmanov Iu B, Lasukova T V, Afanas'ev S A, Maslov L N, Krotenko N M, Naryzhnaia N V
Patol Fiziol Eksp Ter. 1997 Jan-Mar(1):28-31.
Acute cold stress (-20 degrees C for 4 hours) in rats causes profound contractile changes in the heart isolated and perfused by the Langendorf method. This reduced contraction amplitudes and increased heart rates. The decreased contraction amplitudes was associated with inadequate ATP formation. While changing perfusion of post-stress isolated heart, myocardial rigidity slowed down, which seemed to be associated with activated glycolysis. There were no signs of cardiomyocytic lesion after cold stress. Reduced coronary flow is the only abnormal effect of acute cold stress under these conditions. High cardiac resistance to the damaging effect of cold is likely to be related to increased processes of glycolysis and glycogenolysis in the cardiomyocytes.
大鼠急性冷应激（-20℃，4小时）会使通过Langendorf方法分离并灌注的心脏发生显著的收缩变化。这会降低收缩幅度并增加心率。收缩幅度降低与ATP生成不足有关。在改变应激后分离心脏的灌注时，心肌僵硬度减缓，这似乎与糖酵解激活有关。冷应激后没有心肌细胞损伤的迹象。在这些条件下，冠状动脉血流减少是急性冷应激的唯一异常影响。心脏对寒冷损伤作用的高耐受性可能与心肌细胞中糖酵解和糖原分解过程的增加有关。
