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本实验旨在探明变温过程对心肌的影响，以及可能的内在机理。采用阶梯方式降、复温，测定３０℃、２５℃、２０℃、１５℃与１０℃条件下，大鼠乳头肌等长收缩的各参数值的变化。结果表明：在降温过程中，心肌发展张力（ＤＴ）呈双相变化，即从３０℃降温到２５℃，ＤＴ增大，而后ＤＴ逐渐下降；温度降到２０℃时，静息张力（ＲＴ）保持不变，而降至１５℃以后ＲＴ明显上升。乳头肌等长收缩的时间参数如ＴＰＰ、ＴＰＮ、ＴＰＴ、Ｔ１／２Ｒ均随温度的降低而逐渐延长。在复温过程中，与降温过程中相同温度点相比，２０℃、２５℃、３０℃点发展张力明显降低，而１５℃、２０℃、２５℃点静息张力显著增高。这提示在降温过程中，心肌细胞肌钙蛋白Ｃ对Ｃａ２＋敏感性可能呈现双相变化，且低温造成的心肌细胞内游离Ｃａ２＋浓度增高，可能引起心肌细胞损伤。因而，心冷停搏液保护心肌功能的关键环节，应是如何防止在降温过程中心肌细胞内游离Ｃａ２＋浓度一过性增高。
The purpose of this experiment is to investigate the effect of temperature change on myocardium and its underlying mechanism. The step-down and rewarming were used to measure the changes of the isometric contraction of the papillary muscle of rats at 30 ℃, 25 ℃, 20 ℃, 15 ℃ and 10 ℃. The results showed that during the cooling process, the myocardial development tension (DT) showed a biphasic change from 30 ℃ to 25 ℃, DT increased and then DT decreased gradually. When the temperature dropped to 20 ℃, resting tension (RT) Remained unchanged, but dropped to 15 ℃ RT significantly increased. The time parameters of isometric contraction of papillary muscles such as TPP, TPN, TPT, T1 / 2R were gradually prolonged with the decrease of temperature. During the rewarming process, the developmental tension at 20 ℃, 25 ℃ and 30 ℃ decreased significantly compared with that at the same temperature, while the resting tension at 15 ℃, 20 ℃ and 25 ℃ increased significantly. This suggests that in the process of cooling, the sensitivity of cardiomyocyte troponin C to Ca2 + may appear biphasic change, and the increase of intracellular free Ca2 + concentration induced by hypothermia may cause cardiomyocyte injury. Therefore, cardioplegic solution to protect myocardial function of the key link should be how to prevent intracellular free Ca2 + concentration during cooling a transient increase.