Strathprints logo
Strathprints Home | Open Access | Browse | Search | User area | Copyright | Help | Library Home | SUPrimo

Altered oscillatory work by ventricular myofilaments from a rabbit coronary artery ligation model of heart failure

Miller, David J. and MacFarlane, Niall G. and Wilson, Gayle (2003) Altered oscillatory work by ventricular myofilaments from a rabbit coronary artery ligation model of heart failure. Cardiovascular Research, 61 (1). pp. 94-104. ISSN 0008-6363

Full text not available in this repository. (Request a copy from the Strathclyde author)


Objectives: Understanding the changed ability of cardiac myofilaments to produce pump work requires knowledge of kinetics of crossbridge function as well as more widely studied parameters such as Ca-sensitivity and isometric force development. We tested the hypothesis that altered crossbridge kinetics contribute to reduced myofilament work in early-stage heart failure (left ventricular dysfunction, LVD). Methods: The sinusoidal oscillation technique can yield insights into crossbridge function. Dynamic stiffness, oscillatory work and power were assessed in chemically skinned, Ca-activated trabeculae from rabbit ventricles in early-stage failure, 8 weeks after infarction induced by coronary artery ligation (LIG). Results were compared with sham-operated controls (SH). LVD was assessed by echocardiography. Results: Ca-activated force and myofilament Ca-sensitivity were not significantly altered at this early stage of LVD. In maximally Ca-activated preparations, the frequency of minimal dynamic stiffness (fmin) was 23% lower in LIG. fmin increases by >80% between pCa 5.8 and 4 in SH but not in LIG. Maximal phase lead and lag angles (between length and tension) were lower in LIG at frequencies near fmin, lowering oscillatory work and power. The Lissajous figures (oscillatory work loops) of imposed length vs. tension are often asymmetric near fmin. The degree of asymmetry was greater in LIG. Conclusions: Reduced capacity for mechanical power, consistent with depressed haemodynamic performance in LVD hearts, is only partially attributable to crossbridge slowing; changes in the phase relationship will also contribute. These changes are not readily attributable to known alterations in contractile protein isoforms. Some deductions are drawn about which steps in the crossbridge cycle are modified in this model of LVD. Altered cardiac myocyte Ca-transients, reported to be associated with LVD, will be translated into pump work by a contractile machinery that is functionally altered, even though isometric force and myofilament Ca-sensitivity might remain near-normal at this stage.

Item type: Article
ID code: 5518
Keywords: heart failure, contractile function, e-c coupling, ventricular function, rabbit, Physiology, Physiology, Cardiology and Cardiovascular Medicine, Physiology (medical)
Subjects: Science > Physiology
Department: Professional Services > Academic Administration
Related URLs:
    Depositing user: Strathprints Administrator
    Date Deposited: 26 Feb 2008
    Last modified: 04 Sep 2014 15:45

    Actions (login required)

    View Item