论文部分内容阅读
４周的尾部悬吊引起大鼠乳头肌等长收缩发展张力（ＤＴ）降低２９．２％，达到张力峰值的时间（ＴＰＴ）延长１０．４％和舒张一半时间（Ｔ１／２Ｒ）呈降低趋势。解除悬吊１周大鼠的心肌收缩性能并未恢复，其表现为ＤＴ仍降低２４．Ｏ％、ＴＰＴ未见延长，但Ｔ１／２Ｒ却显著地缩短了１３．３％。用ＴｒｉｔｏｎＸ－ｌ００处理乳头肌行干预实验发现，对照大鼠的ＤＴ仅稍降低，而ＴＰＴ与Ｔ１／２Ｒ则明显缩短。与此截然相反，悬吊和恢复大鼠的ＤＴ明显降低，而ＴＰＴ与Ｔ１／２Ｒ却无改变。扫描电镜显示悬吊与恢复大鼠乳头肌内皮细胞核隆起形成的起伏消失，这些均提示模拟失重可能使大鼠心内膜内皮产生一定程度的萎缩或损伤。因此，在探讨模拟失重心血管功能失调变化机理时，心内膜内皮的作用不应忽视。
The 4-week tail suspension resulted in a 29.2% decrease in DT, a 10.4% increase in TPT and a decrease in T1 / 2R . Myocardial contractility did not recover in 1-week-old rats, which showed a decrease in DT. O%, TPT no extension, but T1 / 2R was significantly shortened by 13.3%. TritonX-l00 treatment of papillary muscle line intervention experiments found that control rats DT only slightly reduced, while TPT and T1 / 2R was significantly shorter. In contrast, DT was significantly reduced in both suspended and restored rats, while TPT and T1 / 2R remained unchanged. Scanning electron microscopy showed the disappearance of the ascending and descending nuclei of the papillary muscle cells in suspension and recovery rats, suggesting that simulated weightlessness may cause some atrophy or damage to the endocardial endothelium of rats. Therefore, to explore the mechanism of simulated weight loss cardiovascular dysfunction, the role of endocardial endothelium should not be ignored.