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Force-interval relation in normal and cardiomyopathic hamster atria
S E Howlett1, J Bobet, T Gordon
1Department of Pharmacology, University of Alberta, Edmonton, Canada.
Insights
Cardiomyopathy impairs cardiac muscle contractility by reducing intracellular calcium availability. This study found slower force recovery in cardiomyopathic hearts, indicating beat-to-beat regulation issues.
Area of Science:
- Cardiology
- Cardiac Physiology
- Muscle Biology
Background:
- Cardiomyopathy (CM) is a disease of the heart muscle.
- Understanding beat-to-beat regulation of contractile force is crucial for CM research.
- Calcium handling is a key determinant of cardiac contractility.
Purpose of the Study:
- To investigate the impact of cardiomyopathy on the beat-to-beat regulation of cardiac muscle contractile force.
- To compare contractile function in normal and cardiomyopathic hamster hearts under varying calcium conditions.
Main Methods:
- Isometric force measurements in isolated left atria from normal and cardiomyopathic hamsters.
- In vitro experiments conducted at 29°C with varying external calcium concentrations (2.5 mM and 6.0 mM [Ca2+]e).
- Analysis of force-interval relationships and recovery of steady-state force after rest periods.
Main Results:
- Force was depressed in cardiomyopathic (CM) atria at low external calcium (2.5 mM [Ca2+]e).
- The parameter U(0), reflecting force at short intervals, was lower in CM muscles.
- Recovery of steady-state force after long rest intervals was significantly slower in CM atria (tau = 77.3 s) compared to normal atria (tau = 30.5 s) at high [Ca2+]e (6.0 mM).
Conclusions:
- Cardiomyopathy affects the beat-to-beat regulation of cardiac contractile force.
- Findings suggest reduced availability of intracellular calcium in the cardiomyopathic heart.
- Altered calcium dynamics contribute to contractile dysfunction in cardiomyopathy.
Abstract:
The purpose of this study was to determine how cardiomyopathy affects the beat-to-beat regulation of contractile force in cardiac muscle. Isometric force produced by left atria from 80- to 85-day-old normal and cardiomyopathic (CM) hamsters was measured in vitro at 29 degrees C in 2.5 and 6.0 mM Ca2+. During steady-state stimulation at 1 Hz, single test stimuli were interpolated at varying test intervals (0.3-600 s). The force-interval curves were fitted with an equation using five parameters to define the curve and were compared under different conditions; the recovery of force after long rest intervals was fitted with a single exponential curve. Results showed that the force-interval curves were similar in normal and CM atria except that force was depressed at all intervals in 2.5 mM external Ca2+ concentration ([Ca2+]e) and that the parameter U(0), reflecting force produced at short test intervals, tended to be lower in CM muscles. At high [Ca2+]e (6.0 mM) the force-interval curves were similar, but recovery of steady-state force after long test intervals was much slower in CM atria (tau = 77.3 +/- 8.5 s, n = 11) than in normal atria (tau = 30.5 +/- 3.9 s, n = 11). Recovery was also slower at 2.5 mM [Ca2+]e. These findings suggest that, on a beat-to-beat basis, there is less Ca2+ available in intracellular compartments in the CM heart.