Quantification of Diastolic Viscoelastic Properties of Isolated Cardiac Muscle Cells

Author(s):  
Catalin F. Baicu ◽  
Michael R. Zile

Abstract Pathological processes which cause diastolic congestive heart failure (CHF), such as pressure overload hypertrophy (POH), produce abnormalities in the material properties of cardiac muscle cells (cardiomyocytes) and may selectively alter its elastic stiffness, viscosity, or both. Previous methods used to characterize these cardiomyocyte viscoelastic properties were constrained by specific biological and engineering limitations, which prevented testing in conditions that mimic normal physiology. The current study proposes an uniaxial variable-rate stretching method, in which isolated cardiomyocytes embedded in a three-dimensional gel matrix were subjected to stretch. Physiological Ca++ (2.5 mM) and rapid stretch rates up to 100 μm/sec provided experimental conditions parallel to in vivo physiology. The proposed method identified and individually quantified both cellular stiffness and viscosity, and showed that POH increased both elastic and viscous cardiomyocyte diastolic properties.

1981 ◽  
Vol 241 (4) ◽  
pp. H459-H478 ◽  
Author(s):  
C. O. Lee

Intracellular activities of K, Na, H, Cl, and Ca ions are kept at an optimal level for maintenance of normal cellular functions. Furthermore, many cellular functions are regulated directly or indirectly by these ion activities in cells. The use of ion-selective microelectrodes has emerged as the only method for measuring directly and continuously intracellular ion activities of intact cells. In recent years, they have been extensively used for measurements of intracellular ion activities in cardiac muscle and other tissues. This article concerns both intracellular ion activities of cardiac muscle and intracellular application of ion-selective microelectrodes. Intracellular ion activities in cardiac muscle cells have been measured under several experimental conditions, such as changes in ion composition of bathing fluid and exposure to certain drugs. This approach has provided significant information about electrochemical potentials of ions, membrane transport, and cellular functions related to ion activities. Relevant data and information is presented for K+, Na+, H+, Cl-, and Ca2+. Although ion-selective microelectrodes are widely used, this technique has certain assumptions, problems, and limitations that vary with the types of microelectrodes. The appendix of this article reviews basic principles for intracellular application of ion-selective microelectrodes and examines pertinent assumptions, problems, and issues. Particular features of K+-, Na+-, H+-, Cl--, and Ca2+-selective microelectrodes are described.


1990 ◽  
Vol 87 (11) ◽  
pp. 4275-4279 ◽  
Author(s):  
H. Ito ◽  
S. C. Miller ◽  
M. E. Billingham ◽  
H. Akimoto ◽  
S. V. Torti ◽  
...  

2004 ◽  
Vol 29 (1) ◽  
pp. 83-95 ◽  
Author(s):  
Hung-Chien Wu ◽  
Jaung-Geng Lin ◽  
Chun-Hsien Chu ◽  
Yung-Hsien Chang ◽  
Chung-Gwo Chang ◽  
...  

2005 ◽  
Vol 27 (1) ◽  
pp. 33-51 ◽  
Author(s):  
Ki-Chan Ha ◽  
Han-Jung Chae ◽  
Cheng-Shi Piao ◽  
Suhn-Hee Kim ◽  
Hyung-Ryong Kim ◽  
...  

1981 ◽  
Vol 86 (2) ◽  
pp. 358 ◽  
Author(s):  
M. J. Galvin ◽  
C. A. Hall ◽  
D. I. McRee

Circulation ◽  
2007 ◽  
Vol 116 (suppl_16) ◽  
Author(s):  
Monte Willis ◽  
Rongqin Ren ◽  
Cam Patterson

Bone morphogenetic proteins (BMPs) of the TGF-beta superfamily, have been implicated in multiple processes during cardiac development. Our laboratory recently described an unprecedented role for Bmper in antagonizing BMP-2, BMP-4, and BMP-6. To determine the role of Bmper on cardiac development in vivo, we created Bmper null (Bmper −/−) mice by replacing exons 1 and 2 with GFP. Since Bmper −/− mice are perinatally lethal, we determined pre-natal cardiac function of Bmper −/− mice in utero just before birth. By echocardiography, E18.5 Bmper −/− embryos had decreased cardiac function (24.2 +/− 8.1% fractional shortening) compared to Bmper +/− and Bmper +/+ siblings (52.2 +/− 1.6% fractional shortening) (N=4/group). To further characterize the role of Bmper on cardiac function in adult mice, we performed echocardiography on 8-week old male and female Bmper +/− and littermate control Bmper +/+. Bmper +/− mice had an approximately 15% decrease in anterior and posterior wall thickness compared to sibling Bmper +/+ mice at baseline (n=10/group). Cross-sectional areas of Bmper +/− cardiomyocytes were approximately 20% less than wild type controls, indicating cardiomyocyte hypoplasia in adult Bmper +/− mice at baseline. Histologically, no significant differences were identified in representative H&E and trichrome stained adult Bmper +/− and Bmper +/+ cardiac sections at baseline. To determine the effects of Bmper expression on the development of cardiac hypertrophy, both Bmper +/− and Bmper +/+ sibling controls underwent transaortic constriction (TAC), followed by weekly echocardiography. While a deficit was identified in Bmper +/− mice at baseline, both anterior and posterior wall thicknesses increased after TAC, such that identical wall thicknesses were identified in Bmper +/− and Bmper +/+ mice 1–4 weeks after TAC. Notably, cardiac function (fractional shortening %) and histological evaluation revealed no differences between Bmper +/− and Bmper +/+ any time after TAC. These studies identify for the first time that Bmper expression plays a critical role in regulating cardiac muscle mass during development, and that Bmper regulates the development of hypertrophy in response to pressure overload in vivo.


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