Abstract
REMODELING OF CARDIOMYOCYTE IN CHRONIC ISOPROTERENOL DOSE ADMINISTERED MURINE MODEL

Sanjay Kumar Narang* and Kiran Chauhan

ABSTRACT

β2-Adrenoceptor agonists such as isoproterenol are anabolic in skeletal muscle, and because they promote hypertrophy and improve force producing capacity, they have potential application for enhancing muscle repair after injury. Synthetic β2-adrenoceptor agonists were initially developed for acute asthma treatment, to facilitate bronchiolar smooth muscle dilation. Isoproterenol has been used to treat asthma by opening up the airways in the lungs. Despite their muscle anabolic properties, β-agonists have also been associated with some undesirable side effects, including increased heart rate (tachycardia) and muscle tremor, which have so far limited their therapeutic potential. Since the early 1990s, the use of β-agonists for the purpose of enhancing sporting performance has become increasingly prevalent. In fact, many athletes are not aware of the deleterious cardiovascular effects of chronic high-dose β-agonist administration and in many cases rely on anecdotal information about these compounds from nonscientific sources. The intent of this study is to characterize the effect isoproterenol on healthy murine hearts. Cardiac hypertrophy was commonly observed in mice when were treated chronic doses of β-agonist isoproterenol. In adult mice treated daily with an oral dose of isoproterenol (1.5 mg/kg) for 4 wk, cardiac hypertrophy was observed. The cardiac hypertrophy in isoproterenol-treated mice was associated with an increase in midventricular collagen deposition. Furthermore, it is possible that similar damage can contribute to a deterioration of cardiac functions.

Keywords: Isoproterenol, cardiac muscle, Hypertrophy.


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