Duchenne muscular dystrophy is characterized by a lack of the protein product of the dystrophin gene. Loss of dystrophin interrupts the connection between extracellular matrix and intracellular cytoskeleton. The disease effects skeletal muscle with muscle weakness and degeneration. Cardiac muscle is also affected by the replacement of fibres by fatty tissue. Of the 90% of patients with the disease about 20% develop serious cardiomyopathies resulting in death. Mdx mice lacking dystrophin compare clinically to the human form. Crude sample preparation was carried out on total cardiac mouse muscle. Reagents for lysis buffers were chosen based on their effects, such as solubility, ability to act as reducing agent or reaction with other buffer components. Variations in these buffers were used to determine the electrophoretic effect on cardiac proteins. Separation was carried out by 2D-gel electrophoresis. Staining was carried out with colloidal commassie and proteins of interest were identified by MALDI-ToF mass spectrometry. Research was supported by IRCSET.