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Reverse chamber remodelling following adrenergic-induced advanced cardiac dilatation and pump dysfunction
Hendrik L Booysen1, Gavin R Norton, Lionel H Opie
1Cardiovascular Pathophysiology and Genomics Research Unit, Faculty of Health Sciences, School of Physiology, University of the Witwatersrand Medical School, 7 York Road, Parktown, Johannesburg, 2193, South Africa.
Basic Research in Cardiology
|December 23, 2011
Summary
Stopping excessive beta-adrenergic receptor stimulation, like with isoproterenol (ISO), can fully reverse cardiac dilatation and pump dysfunction. Even with cardiomyocyte apoptosis, removing the stimulus allows heart function and structure to normalize in rats.
Area of Science:
- Cardiovascular Physiology
- Pharmacology
- Cell Biology
Background:
- Adrenergic-induced cardiac dilatation is linked to cardiomyocyte death.
- The reversibility of established cardiac dysfunction after excessive adrenergic stimulation is not fully understood.
Purpose of the Study:
- To investigate if withdrawing beta-adrenergic receptor agonist (isoproterenol) reverses cardiac dilatation and pump dysfunction in rats.
- To assess the impact on cardiomyocyte apoptosis and myocardial necrosis.
Main Methods:
- Rats received daily isoproterenol (ISO) for 6 months to induce cardiac dilatation and dysfunction.
- ISO was withdrawn for 4 months in a subset of rats (ISO + recovery group).
- Cardiac structure, function (e.g., left ventricular diameters, contractility), cardiomyocyte apoptosis, and myocardial necrosis were assessed.
Main Results:
- Chronic ISO administration significantly increased left ventricular volumes and decreased contractility.
- While ISO induced cardiomyocyte apoptosis, it did not cause myocardial necrosis.
- Withdrawal of ISO for 4 months resulted in complete normalization of cardiac dimensions and function, similar to control rats.
Conclusions:
- Excessive beta-adrenergic stimulation causes significant cardiac dilatation and dysfunction.
- Complete reversal of cardiac dilatation and pump dysfunction is achievable by withdrawing the adrenergic stimulus, even with concurrent cardiomyocyte apoptosis.
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