摘要
采用离体乳头肌灌流、改变刺激频率和快速冷却等干预实验,探讨模拟失重4周大鼠心肌收缩性能降低的可能机理。结果表明:模拟失重大鼠乳头肌:(1)等长收缩达到张力峰值的时间明显延长;(2)细胞外Ca+浓度为8.0mmol/L时,增加刺激频率,张力随之降低;(3)电刺激张力与停止电刺激ls的冷挛缩张力明显降低。这些均提示,模拟失重4周可能使心肌肌浆网Ca++摄取与释放速率降低。
The purpose of this study
was to assess the function of cardiac sarcoplasmic reticuium in rats during simulated
weightlessness. After 4 weeks of tail-suspension ,the isolated left ventricular papillary muscle
showeda significant decrease in isometric contrac-tion tension(2.30±0.15 vs.3. 25±
0.22g/mm2P<0.01), and a prolongation in time to peak tension (141.3±2.9vs. 128.O±3.6 ms
P<0.05). When extracellular Ca++concentration of the papillary preparation was controlled at 8.
0mmol/L, tension was decreased with increase of stimulation frequency in tail-suspended rats.
Further-more,the ESC/RCC60 and RCC1/RCC60 were reduced in rapid cooling contracture test in
tail-suspended rats. These results suggest that simulated weightlessness for 4 weeks may
depress the rate of Ca++ release and uptake in cardiac sarcoplasmic reticulum.
出处
《航天医学与医学工程》
CAS
CSCD
1994年第4期279-284,共6页
Space Medicine & Medical Engineering
基金
国家自然科学基金
关键词
模拟失重
心肌收缩性
乳头肌
肌浆网
simulated Weightlessness, myocardium contractility, papillary musele,sar-coplasmic reticulum