模拟失重可能损害心内膜内皮

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。

Endocardial Endothelium May be Harmed by Simulated Weightlessness

The role of endocardial endothelium(EE) in intracavitary autoregula-tion of cardiac performance has now been well demonstrated. We tested the hypothesisthat whether EE is involved in cardiovascular deconditioning caused by simulated weight-lessness. The contractile performance of papillary muscles before and after selective re-moval of EE by Triton X-100 from 4-week tail-suspension(SUS-4),4-week suspensionand 1-week recovery(RE-1) and synchronous control(CON) SD rats(25O-300g) wereinvestigated. The surface structure of EE of papillary muscles from the three groups wereexamined by scanning electron microscopy. Results showed that 4-week tailsuspensioncaused a 29.2% decrease in the developed tension(DT)(P<0.01), a 10.4% prolon-gation of time to peak tension(TPT)(P<.05), and a shortening trend of time to halfrelaxation ( T1 / 2R ). DT was still depressed by 24.0%and T1/ 2R was shortened by13.3% in RE-1 group. After the Triton X-100 treatment, there was no significantchange in DT, but shortening in TPT and T1/2R was found in CON group; there weresignlficant decrease in DT, but no significant changes in TPT and T1/2R in SUS-4 andRE-1 groups. In SUS-4 and RE-1 groups, the appearance of surface undulation formedby bulging nuclei disappeared in scanning electron microscopy. It means that there maybe atrophic changes of EE. It is suggested that EE might be involved in cardiovascular de-conditioning caused by simulated weightlessness.