模拟失重大鼠心肌收缩性能降低涉及细胞钙转运机制  

DEPRESSED CARDIAC CONTRACTILIY INVOLVES MYOCARDIAL CALCIUM TRANSPORTATION IN SIMULATED WEIGHTLESS RATS

作　　者：余志斌[1] 张立藩[1] 陈杰[1] 

机构地区：[1]西安第四军医大学航空生理学教研室

出　　处：《中国应用生理学杂志》1995年第2期97-101,共5页Chinese Journal of Applied Physiology

摘　　要：本研究采用离体乳头肌灌流技术，观察了模拟失重４周大鼠心肌收缩性能的变化。同时采取改变细胞外液中Ｃａ￣（２＋）浓度，用Ｌａ￣（３＋）置换细胞膜部位Ｃａ￣（２＋）、以及快速冷却等干预实验方法，探讨模拟失重大鼠心肌收缩性能发生改变的可能机制。结果表明：模拟失重大鼠乳头肌钙反应的ＥＣ＿（５０）值无显著改变，但其发展张力的幅值却明显降低；用ＬａＣｌ＿３灌流使发展张力降低５０％所需时间明显缩短；冷挛缩实验中的ＥＳＣ／ＫＣＣ＿（６０）与ＲＣＣ＿１／ＫＣＣ＿（６０）比值也显著降低。这些均提示模拟失重大鼠心肌收缩性能降低可能与心肌细胞的钙转运功能受损有关。Usign isolated papillary muscle perfusion ,the influence of simulated weightlessness for 4 weeks on myocardial contractility of rat was observed.In the meantime,the effects of interferingtests,such as changing extracellular Ca￣(2+) concentration,displacing membrane-bound Ca￣(2+) bylanthanum(La￣3+))and reducing rapidly temperature of perfusion,on contractility were studied.The results showed that the EC_(50)([Ca￣(2+)]。at 50% relative tension) for calcium in simulatedweightless rats myocardium was 1.06 ± 0.04mmol / L which was not different from that of con- trol,but its developed tension decreased at any extracellular Ca￣(2+) concentration. The time for tension decrease to 1 / 2 during La￣(3+) perfusion was significantly shortened in simulated weightless rats.The ESC / RCC_(60) and RCC _1 / RCC_(60) were reduced in rapid coolingcontracture. These results suggest that simulated weightlessness may damage myocardial calcium transportation.

关 键 词：模拟失重 细胞钙转运 心肌 收缩 

分 类 号：R852.22[医药卫生—航空、航天与航海医学]