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Updated: Jul 14, 2026
Rodent Working Heart Model for the Study of Myocardial Performance and Oxygen Consumption
Published on: August 16, 2016
Effects of complete heart block on myocardial function, morphology, and energy metabolism in the rat
S Gizurarson1, M Lorentzon, T Råmunddal
1Department of Cardiology and Wallenberg Laboratory at Sahlgrenska Academy, Bruna stråket 16, 413 45 Gothenburg, Sweden.
Insights
Complete heart block (CHB) in rats caused significant cardiac enlargement but no heart failure. This model is valuable for studying bradycardia effects on heart function and metabolism.
Area of Science:
- Cardiology
- Physiology
- Biochemistry
Background:
- Severe bradycardia can lead to congestive heart failure (CHF).
- Understanding the chronic effects of complete heart block (CHB) on cardiac function is crucial.
Purpose of the Study:
- To investigate the acute and chronic effects of CHB on cardiac function, morphology, and creatine metabolism.
- To establish a rat model for studying CHB and bradycardia.
Main Methods:
- CHB was induced in rats via electrocautery of the AV node.
- Transthoracic echocardiography and invasive hemodynamic assessments were performed at 1, 3, and 12 weeks.
- Myocardial creatine and high-energy phosphometabolites were analyzed post-sacrifice.
Main Results:
- CHB rats exhibited a ~50% decrease in heart rate and a 2.5-fold increase in stroke volume.
- Despite marked cardiomegaly and biventricular dilatation, CHB rats showed no signs of CHF.
- Myocardial creatine and phosphometabolite levels remained unchanged.
Conclusions:
- Rats with CHB compensate for reduced heart rate with increased stroke volume.
- This CHB rat model is suitable for studying bradycardia's impact on myocardial structure, function, and metabolism.
- The model may aid research into cell therapies for atrioventricular conduction disorders.
Aims:
Severe sustained bradycardia may cause acute and possibly chronic congestive heart failure (CHF). The aim of this study was to investigate acute and chronic effects of complete heart block (CHB) on cardiac function, morphology, and creatine (Cr) metabolism.
Methods And Results:
CHB was induced in male Sprague-Dawley rats (approximately 250 g, n = 11) by means of electrocautery applied to the region of AV node and were compared with controls (n = 15). The rats were investigated at 1, 3, and 12 weeks after CHB induction with transthoracic echocardiography. Invasive haemodynamic assessment of left and right ventricular pressures was performed at 12 weeks. After the sacrifice, the hearts were freeze-clamped for analysis of myocardial Cr, and high energy phosphometabolites. The efficacy of operative procedure was 54%. The peri-operative mortality rate was 20%. Heart rate (HR) decreased by approximately 50% (P < 0.01) while stroke volume (SV) increased 2.5 times (P < 0.01) in the CHB rats. Cardiac index remained unchanged. The rats with CHB grew normally and were in no apparent distress. Filling pressures in left and right ventricles were normal. The CHB rats developed marked cardiomegaly with biventricular dilatation and eccentric left ventricular hypertrophy (P < 0.01). There was no change in the myocardial content of Cr and high energy phosphometabolites.
Conclusion:
Rats with CHB are compensating for reduction in HR with increased SV without haemodynamic and biochemical characteristics of CHF. This model may be useful to study the effects of CHB and bradycardia on myocardial structure, function, electrophysiology, and metabolism as well as for studies of cell therapy for reparation of AV conductance.
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