Morphological and functional characteristics of models of experimental myocardial injury induced by isoproterenol

Abstract

Abstract. The animal models of myocardial injury induced by systemic β-adrenergic receptor agonist administration represent an experimental approach of persisting interest. These models were found useful especially for studies of structural and functional adaptation of myocardium during the progression of cardiac adaptive response towards maladaptive hypertrophy and insufficiency. The pathological alterations induced by isoproterenol (ISO) do not develop evenly. The ISO models may contribute effectively to understanding of pathologies in signal transduction, energetics, excitability and contractility that may contribute concomitantly to cardiac dysfunction and heart failure. In this minireview we focused on the alterations in general characteristics and heart function as well as on the morphological changes of cardiomyocytes developed during ISO administration. The morphological alterations within the cellular macro-and microdomains correspond to the electrical remodeling and contractile dysfunction of ventricular myocardium that could be used to identify pathological changes ranging from hypertrophy to failing heart.

Mitochondrial disruption occurs downstream from β-adrenergic overactivation by isoproterenol in differentiated, but not undifferentiated H9c2 cardiomyoblasts: Differential activation of stress and survival pathways

“…Isoproterenol-induced β-adrenergic overload leads to cardiac cell dysfunction, which is a good example of chemically-induced heart toxicity and failure (Nichtova et al, 2012).…”

PEG-coated gold nanoparticles attenuate β-adrenergic receptor-mediated cardiac hypertrophy

“…15 Thus isoproterenol (ISO), the agonist of β-AR, has been widely used to establish the animal model of cardiac hypertrophy. 16,17 ISO is reported to induce both chronic and acute cardiac hypertrophy in animal experiments. The chronic cardiac hypertrophy model is used to simulate the chronic progression of heart remodeling in some chronic cardiovascular diseases such as hypertension.…”

Relaxin Family Member Insulin‐Like Peptide 6 Ameliorates Cardiac Fibrosis and Prevents Cardiac Remodeling in Murine Heart Failure Models

“…Consistent with other studies under the conditions of our assays,26 we find that low doses of AngII infusion in WT mice induced significant cardiac hypertrophy without causing significant cardiac systolic failure. Isoproterenol acts on β‐adrenergic receptors, resulting in increased heart rate and cardiac overload 25, 26. Consequently, increased myocardium oxygen demand and stress results in cardiac remodeling accompanied by myocardial necrosis, hypertrophy, and fibrosis 25, 44.…”

“…Isoproterenol acts on β‐adrenergic receptors, resulting in increased heart rate and cardiac overload 25, 26. Consequently, increased myocardium oxygen demand and stress results in cardiac remodeling accompanied by myocardial necrosis, hypertrophy, and fibrosis 25, 44. In this study, we found that a moderate‐dose isoproterenol treatment resulted in LV systolic dysfunction and fibrosis without inducing cardiac hypertrophy.…”

“…The isoproterenol‐induced cardiac injury model was used, as previously reported 23, 24, 25. Briefly, isoprenaline hydrochloride (I5627; Sigma‐Aldrich) dissolved in sterile saline at 50 mg/mL was filtered via a 20‐μm filter.…”