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Updated: Jul 22, 2026
Acute Myocardial Infarction in Rats
Published on: February 16, 2011
Congestive heart failure after myocardial infarction in the rat: cardiac force and spontaneous sarcomere activity
A W Davidoff1, P A Boyden, K Schwartz
1Department of Medicine, Faculty of Medicine, University of Calgary, Calgary, Alberta, T2N 4N1 Canada.
Insights
Congestive heart failure (CHF) involves increased spontaneous diastolic sarcomere length fluctuations, potentially altering cardiac function. This study suggests a novel mechanism involving SR Ca(2+) channel activity in CHF pathophysiology.
Area of Science:
- Cardiology
- Physiology
- Molecular Biology
Background:
- Reduced cardiac force development is a hallmark of congestive heart failure (CHF), but its underlying subcellular mechanisms remain unclear.
- Myocardial infarction (MI) can lead to CHF, yet the specific cellular changes contributing to contractile dysfunction are not fully elucidated.
Purpose of the Study:
- To investigate the subcellular mechanisms responsible for decreased force development in rat hearts with congestive heart failure (CHF) post-myocardial infarction.
- To compare the properties of cardiac trabeculae from rats with CHF (cMI) to those with a myocardial scar but no CHF (uMI) and sham-operated controls.
Main Methods:
- Assessment of cardiac function in rat models of myocardial infarction, categorizing animals into CHF (cMI), uncompensated scar (uMI), and sham groups.
- Analysis of trabeculae properties, including maximal twitch force, post-extrasystolic potentiation, calcium sensitivity ([Ca(2+)](o)), and spontaneous diastolic sarcomere length fluctuations (SA).
Main Results:
- Maximal twitch force after post-extrasystolic potentiation was unchanged in cMI trabeculae.
- Increased sensitivity to extracellular calcium ([Ca(2+)](o)) was observed in cMI trabeculae.
- Spontaneous diastolic sarcomere length fluctuations (SA) were elevated in cMI at all levels of sarcoplasmic reticulum (SR) Ca(2+) loading and were proportionally linked to reduced maximal force (F(max)).
Conclusions:
- The findings suggest an increased probability of spontaneous diastolic opening of SR Ca(2+) channels in CHF.
- This mechanism may underlie systolic and diastolic dysfunction and arrhythmias observed in CHF.
- Further investigation into SA in human CHF could significantly impact therapeutic strategies.
Abstract:
The causes of reduced cardiac force development in congestive heart failure (CHF) are still uncertain. We explored the subcellular mechanisms leading to decreased force development in trabeculae from rats with a myocardial infarction. We defined CHF according to clinical and pathological criteria and compared properties of trabeculae from animals with CHF (cMI) to those of animals with a myocardial scar but without evidence of CHF (uMI), and sham-operated animals. The new findings of this study on properties of cMI trabeculae are that (1) maximal twitch force following post-extrasystolic potentiation is unchanged; (2) the sensitivity of cMI trabeculae to [Ca(2+)](o) is increased; (3) spontaneous diastolic sarcomere length (SL) fluctuations (SA) are increased in cMI at all levels of SR Ca(2+) loading; and (4) SA is accompanied by a proportional reduction of F(max). The results suggest that the probability of spontaneous diastolic opening of SR Ca(2+) channels is increased in CHF. These data provide the basis for a novel mechanism underlying systolic and diastolic dysfunction as well as arrhythmias in hearts in CHF. If SA proves to be a component of myocardial dysfunction in human CHF, our thinking about therapy of the patient with CHF may be profoundly changed.
