全部 标题 作者
关键词 摘要

OALib Journal期刊
ISSN: 2333-9721
费用:99美元

查看量下载量

相关文章

更多...
-  2017 

心肌肥厚和心力衰竭时左心室收缩力及钙瞬变的变化 Changes of the Contraction and Calcium Transients in Myocytes of Left Ventricle in Patients with Cardiac Hypertrophy and Heart Failure

Keywords: 心肌肥厚,心力衰竭,钙瞬变,肌小节收缩

Full-Text   Cite this paper   Add to My Lib

Abstract:

目的:研究心肌肥厚和心力衰竭时左心室收缩力及钙瞬变的变化。方法:采用主动脉缩窄术构建压力负荷型心衰小鼠模型及心肌肥厚小鼠模型,小动物超声机测量小鼠心室壁厚度及射血分数,Langendorff灌流术分离小鼠左心室心肌细胞,高速CCD摄像机系统和双激发荧光倍增系统同步测量左心室心肌细胞肌小节收缩舒张功能和胞内钙瞬变。结果:与假手术组相比,肥厚小鼠心室壁明显增厚,胞质基础钙浓度、钙瞬变振幅增高,钙瞬变达峰时间、恢复时间和肌小节舒张时间明显延长,肌小节初长度缩短;心衰组小鼠心腔扩大,射血分数(EF)、钙瞬变峰值、峰高、达峰时间及胞质内钙恢复的速度明显下降,肌小节初始长度显著缩短,收缩幅度下降,静息期基础钙浓度显著上升,收缩及舒张时间均明显延长。结论:在心力衰竭的发展过程中,随着心脏结构的改变,心肌细胞对胞内钙的释放和回收能力均下降,使单个心肌细胞收缩无力、舒张时间延长,进而影响整个心脏的收缩舒张功能。改善心肌细胞钙循环可能在缓解心衰患者临床症状和改善预后方面起到关键作用

References

[1]  Lopez-Lopez JR,Shacklock PS,Balke CW,et al.Local,stochastic release of Ca2+in voltage-clamped rat heart cells:Visualization with confocal microscopy[J].J Physiol,1994,480(Pt 1):21-29.
[2]  Yao A,Matsui H,Spitzer KW,et al.Sarcoplasmic reticulum and Na+/Ca2+exchanger function during early and late relaxation in ventricular myocytes[J].Am J Physiol,1997,273(6Pt 2):H2 765-H2 773.
[3]  Rebbeck RT,Karunasekara Y,Board PG,et al.Skeletal muscle excitation-contraction coupling:Who are the dancing partners[J]?Int J Biochem Cell Biol,2014,48:28-38.
[4]  Horiuchi-Hirose M,Kashihara T,Nakada T,et al.Decrease in the density of t-tubular l-type Ca2+channel currents in failing ventricular myocytes[J].Am J Physiol Heart Circ Physiol,2011,300(3):H978-H988.
[5]  Hu ST,Liu GS,Shen YF,et al.Defective Ca2+handling proteins regulation during heart failure[J].Physiol Res,2011,60(1):27-37.
[6]  Cheng J,Xu L,Lai D,et al.Camkii inhibition in heart failure,beneficial,harmful,or both[J].Am J Physiol Heart Circ Physiol,2012,302:H1 454-H1 465.
[7]  Diwan A,Wansapura J,Syed FM,et al.Nix-mediated apoptosis links myocardial fibrosis,cardiac remodeling,and hypertrophy decompensation[J].Circulation,2008,117(3):396-404.
[8]  Curran J,Tang L,Roof SR,et al.Nitric oxide-dependent activation of camkii increases diastolic sarcoplasmic reticulum calcium release in cardiac myocytes in response to adrenergic stimulation[J].PLoS One,2014,9(2):e87495.
[9]  Clay SA,Domeier TL,Hanft LM,et al.Elevated Ca2+transients and increased myofibrillar power generation cause cardiac hypercontractility in a model of noonan syndrome with multiple lentigines[J].Am J Physiol Heart Circ Physiol,2015,308(9):H1 086-H1 095.
[10]  Sullivan MJ,Knight JD,Higginbotham MB,et al.Relation between central and peripheral hemodynamics during exercise in patients with chronic heart failure.Muscle blood flow is reduced with maintenance of arterial perfusion pressure[J].Circulation,1989,80(4):769-781.
[11]  Ibrahim M,Navaratnarajah M,Siedlecka U,et al.Mechanical unloading reverses transverse tubule remodelling and normalises local calcium-induced calcium release in a rodent model of heart failure[J].Eur J Heart Fail,2012,14(6):571-580.

Full-Text

Contact Us

service@oalib.com

QQ:3279437679

WhatsApp +8615387084133