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A Rat Model of Pressure Overload Induced Moderate Remodeling and Systolic Dysfunction as Opposed to Overt Systolic Heart Failure
Published on: April 30, 2020
Slow contractions characterize failing rat hearts
Janny Bøkenes1, Jan Magnus Aronsen, Jon Arne Birkeland
1Institute for Experimental Medical Research, Ullevaal University Hospital, 0407, Oslo, Norway. janny.bokenes@medisin.uio.no
Basic Research in Cardiology
|March 19, 2008
Summary
Congestive heart failure (CHF) in rats shows altered cardiomyocyte function. Electrical remodeling impacts contraction force, while different mechanisms slow heart muscle contraction speed.
Area of Science:
- Cardiology
- Cellular Biology
- Physiology
Background:
- Heart failure is characterized by reduced cardiac contractility and slower contraction.
- The underlying cellular mechanisms for these deficits are not fully understood.
Purpose of the Study:
- To investigate the distinct cellular mechanisms responsible for reduced force and slower contraction in a rat model of post-infarction congestive heart failure (CHF).
Main Methods:
- In vivo measurements of ECG, echocardiography, and left ventricular (LV) pressure.
- In vitro assessment of contraction parameters (shortening, velocity) in isolated LV cardiomyocytes under various stimulation protocols.
- Analysis of electrical remodeling, including action potentials (AP) and diastolic membrane potential (DMP).
Main Results:
- CHF rats exhibited decreased LV systolic pressure and +dP/dtmax, with prolonged systolic duration.
- Isolated CHF cardiomyocytes showed depolarized action potentials and prolonged AP duration.
- Increased fractional shortening (FS) in CHF cells correlated with sarcoplasmic reticulum Ca2+ load and electrical remodeling.
- Time to peak contraction (TTP) was prolonged in CHF cells but less affected by electrical remodeling, indicating distinct mechanisms for contraction slowing.
Conclusions:
- Electrical remodeling, specifically altered diastolic membrane potential and action potential duration, significantly influences the force of cardiomyocyte contraction in CHF.
- The mechanisms responsible for the slowed contraction in CHF are separate from those affecting contraction force.
