The transformants were screened for the presence of plasmids by S1-PFGE and their resistance phenotypes were determined. The sizes of the cfrcarrying plasmids extracted from the transformants were estimated by calculation of the sums of the different fragment sizes obtained after BglII digestion. In Duchenne muscular dystrophy the absence of dystrophin causes subclinical or clinical dilated cardiomyopathy. Also, mutations in one of the genes for a-, b-, c- ord-sarcoglycan, a heterogeneous group of autosomal recessive limb girdle muscular dystrophies, cause severe dilated cardiomyopathy at a young age in addition to muscular dystrophy, especially in those patients with LGMD2F caused by mutations in the d-sarcoglycan gene. Beta-blockers are established treatments for acquired heart failure though the role in inherited cardiomyopathies is less clear. It has been suggested that for certain dystrophin mutations which predispose to cardiomyopathy, early treatment including beta-blockers is of benefit. We have shown that in mdx mice, which lack the protein dystrophin as in Duchenne muscular dystrophy that there are benefits in terms of left ventricular pressure-volume AbMole Brusatol derived data with early beta- blocker treatment, though detrimental effects in the delta sarcoglycan deficient mouse model. This suggests that not all underlying genotypes may respond beneficially to beta-blockers. AbMole Seratrodast However, left ventricular pressure and volume measurements are not the only physiological measurements that can assess the effects of a systemic treatment. Right ventricular function is frequently abnormal in cardiomyopathy. Both left and right ventricular function can be assessed non-invasively with cardiac magnetic resonance imaging. Increased intracellular calcium is an important feature of muscular dystrophy cardiomyopathy and plays a central role in its pathophysiology. Manganese-enhanced magnetic resonance imaging can assess in-vivo calcium influx using 2 properties of the manganese ion. Manganese enters cardiomyocytes through calcium channels, and is also a T1 contrast agent with MRI. Thus, manganese influx results in a relative increase in contrastenhancement on T1 weighted images. The purpose of this study was to treat 2 different mouse models of muscular dystrophy cardiomyopathy with beta-blockers at an early stage in the development of the cardiomyopathy to determine if there are beneficial effects on left and right ventricular function and to determine whether beta-blockers reduced in-vivo myocardial calcium influx. In two mouse models of muscular dystrophy cardiomyopathy treated with the beta-blocker metoprolol at an early stage in the development of the cardiomyopathy, we show that there are differences in left and right ventricular function and the responses to treatment. In the mdx mice without treatment there is ventricular hypertrophy, reduced left ventricular stroke volume with a small left ventricular cavity size, normal left ventricular ejection fraction but reduced right ventricular ejection fraction. Consistent with our previous invasive catheter based studies there are benefits of metroprolol on left ventricular function in the mdx mice, but here we also demonstrate deterioration in right ventricular function. The Sgcd-/- mice develop ventricular hypertrophy with metoprolol, but have normal left and right ventricular function without treatment with no significant effects of treatment on left or right ventricular function relative to C57 Bl10 mice.