摘要
为研究模拟失重对大鼠心肌肌浆网Ca2+摄取功能的影响,采用差速离心法制备心肌肌浆网(CSR)粗制膜,测定CSR囊泡膜各种ATP酶活性,并用Millipore滤过技术测定CSR囊泡的Ca2+摄取功能。结果表明,4周模拟失重大鼠心肌肌浆网膜Ca2+,Mg2+-ATP酶活性不变,Ca2+-激活ATP酶活性却较对照组降低6.8%(P<0.05)。模拟失重组心肌肌浆网囊泡ATP依赖性Ca2+摄取的时间动态曲线较对照组降低19%~31%(P<0.05或P<0.01)。在测定的Ca2+浓度范围内,Ca2+依赖性Ca2+摄取速率较对照组减低19%~39%(P<0.05或P<0.01)。对照组与模拟失重组的Ca/P耦联比值分别为0.22±0.06与0.20±0.09,两值间无显著差别(P>0.05)。结果提示,这可能是模拟失重导致心肌等长收缩发展张力幅值降低与达到张力峰值时间(TPT)延长的内在机理之一。
Crude cardiac sarcoplasmic reticulum(CSR ) membrane vesicles
were prepared by differen-tial centrifugation. Its ATPase activity and Ca2+uptake function were
assayed and examined. Ca2+uptake was determined by a Millipore filter technique with Ca2+ as
an isotopic tracer. As compared with the controls,Ca2+,Mg2+-ATPase activity didn’t show any
significant change,whereas CSR Ca2+-activated ATPase activity showed a 6.8% decrease
(P<0.05) in 4-week tail-suspension.Results concerning changes in CSR Ca2+ uptake during
simulated weightlessness showed that, the ini-tial rate of Ca2+ uptake of CSR preparation was
decreased by 19.0%(P<0.05),the curve of time course of Ca2+ uptake shifted downwards, and
the Ca2+-dependent Ca2+ uptake was decreased by 19~39%(P<0.05 or P<0. 01)as compared
with that of the control rats.The apparent coupling ratio of Ca2+ uptake to Ca2+ -ATPase
activity didn’t show any significant difference(P>0.05) between the two groups. These results
suggest that lowered CSR Ca2+ uptake might be one of the underlying mechanisms leading to
reduced developed tension and prolonged time to peak tension in isometric con-traction of
papillary muscle from 4-week tail-suspended rats.
出处
《航天医学与医学工程》
CAS
CSCD
1995年第2期84-88,共5页
Space Medicine & Medical Engineering
基金
国家自然科学基金
关键词
失重模拟
心肌收缩
腺苷三磷酸酶类
大鼠
weightlessness simulation
myocardial contraction adenosinetriphosphatase rats Address reprint requests to : YU Zhibin.
Department of Aerospace Physiology,The Fourth Military Medical University,Xi’an 710032