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观察了尾部悬吊40d和120d大鼠心肌超微结构的变化。结果显示，40d悬吊大鼠心肌细胞浆内糖原增加；心肌毛细血管内皮细胞生成了许多凸出物伸向管腔内。这些改变与空间实验室及宇宙号生物卫星搭载航天大鼠心肌超微结构变化基本一致，而与以往在地面用应激程度严重的“禁动”模型所观察的变化有所不同。此外，我们还发现120d悬吊大鼠心肌细胞内脂褐素增加，这在以往航天及地面模拟研究中均未见报道，可能是长期失重或模拟失重下心肌超微结构变化的重要特点之一。上述形态学改变可归结为两方面的问题，即心肌糖酵解过程受到抑制和心肌组织的降解过程增强。从而支持长期模拟失重大鼠的心脏处于低动力状态的假说。
The ultrastructural changes in myocardium were observed at 40d and 120d after tail suspension. The results showed that the plasma glycogen increased in the cardiomyocytes of the 40-day-old rats, and many of the endothelial cells of the cardiomyocytes developed into the lumen. These changes are basically consistent with the ultrastructural changes of the myocardium of aerospace rats carried by space laboratories and cosmic cosmic satellites, and they are different from the changes observed in the “forbidden” model that used to be heavily stressed on the ground in the past. In addition, we also found that the increase of lipofuscin in myocardial cells of 120 d suspended rats was not reported in the past aerospace and ground simulation studies, which may be one of the important features of myocardial ultrastructure changes under long-term weightlessness or simulated weightlessness . The above morphological changes can be attributed to two problems, namely, inhibition of cardiac glycolysis and enhancement of myocardial tissue degradation process. Thus supporting the hypothesis that the heart of a rat simulating long-term weightlessness is in a low motility state.