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Updated: Jun 21, 2026
Cell-based Therapy for Heart Failure in Rat: Double Thoracotomy for Myocardial Infarction and Epicardial Implantation of Cells and Biomatrix
Published on: September 22, 2014
Effects of therapy using the Celacade system on structural and functional cardiac remodelling in rats following
Mei Luo Zhang1, Jie Mei, Lori Anne Archer
1Department of Cardiovascular Sciences, Libin Cardiovascular Institute of Alberta, Faculty of Medicine, University of Calgary, Calgary, Alberta T2N 4N1.
Insights
Celacade treatment in rats with myocardial infarction (MI) reduced transforming growth factor beta-1 during the acute phase and improved cardiac function. However, it did not prevent long-term cardiac dilation after MI.
Area of Science:
- Cardiovascular Research
- Immunomodulation
- Myocardial Infarction
Background:
- The Celacade system modulates the immune response, showing potential in reducing mortality and hospitalizations in human heart failure.
- Investigating Celacade's effects on cardiac function and inflammatory markers post-myocardial infarction (MI) is crucial for understanding its therapeutic potential.
Purpose of the Study:
- To evaluate the impact of Celacade on acute cytokine expression following coronary artery ligation in rats.
- To assess cardiac dimensions and systolic/diastolic function in rats after myocardial infarction (MI) with Celacade treatment.
Main Methods:
- Celacade was administered pre-surgery and monthly post-coronary artery ligation in a rat model.
- Cytokine expression was measured via ELISA, echocardiograms assessed cardiac dimensions, and mechanical properties of cardiac muscle (force, sarcomere length) were analyzed.
Main Results:
- Celacade inhibited transforming growth factor beta-1 production in the infarct area on day 7.
- While Celacade did not prevent cardiac dilation, it restored positive inotropism and reduced diastolic dysfunction in MI rats.
Conclusions:
- Celacade effectively reduces acute transforming growth factor beta-1 expression post-MI in rats.
- Celacade improves cardiac contractility and diastolic function in MI rats, despite not preventing chronic dilation.
Background:
Immune modulation by the Celacade system (Vasogen Inc, Canada) decreases mortality and hospitalization in human heart failure.
Objectives:
To study the effects of Celacade in rats on acute cytokine expression after coronary artery ligation, cardiac dimensions following myocardial infarction (MI), and systolic and diastolic function of cardiac muscle in MI.
Methods:
Celacade treatment was administered 14 days before coronary artery ligation and monthly after the surgery. Cytokine expression in cardiac tissue was measured on days 1 and 7 by ELISA in sham rats and in rats with MI (with or without Celacade treatment). Echocardiograms were obtained serially for 16 weeks. Force and sarcomere length (SL) were measured by strain gauge and laser diffraction in isolated right ventricle trabeculas at 16 weeks. The inotropic effect of pacing on force was quantified as F5 Hz/0.5 Hz. Diastolic dysfunction was quantified as the root mean square of spontaneous SL fluctuations.
Results:
Celacade inhibited transforming growth factor beta-1 production in the infarct area on day 7 (191.6+/-22.6 pg/mg versus 275.4+/-30.1 pg/mg; P<0.05), but did not attenuate cardiac dilation in MI. Celacade restored positive inotropism of pacing in MI (F5 Hz/0.5 Hz in Celacade, 219.1+/-46.7%; MI, 148.1+/-27.1% [P<0.05 compared with 211.4+/-37.9% in sham]). Celacade reduced diastolic dysfunction in MI (root mean square of spontaneous SL fluctuations: 121+/-15% and 143+/-19% with Celacade versus 184+/-19% and 190+/-26% without Celacade at 26 degrees C and 36 degrees C, respectively) compared with sham (100%; P<0.05).
Conclusions:
Celacade reduces the increase of transforming growth factor beta-1 expression during the acute stage of MI in rats, but does not prevent chronic cardiac dilation. Celacade restores the positive inotropic effect of increased pacing rate in trabeculas from rat right ventricles with large MIs and reduces diastolic dysfunction.
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