We have shown previously that burn trauma produces significant cardiac dysfunction, which is first evident 8 hours postburn and is maximal 24 hours postburn. Since calcium handling by the cardiomyocyte is essential for cardiac function, one mechanism by which burn injury may cause cardiac abnormalities is via calcium dyshomeostasis. We hypothesized that major burn injury alters cardiomyocyte calcium handling through changes in calcium transporter expression. Sprague-Dawley rats were given either burn injury or no burn injury (controls). Cardiomyocyte intracellular calcium and sodium were quantified at various times postburn using Fura-2AM or SBFI fluorescent indicators, respectively. In addition, hearts freeze-clamped at various times postburn (2, 4, 8, and 24 hours) were used for Western blot analysis using antibodies against the sarcoplasmic reticulum Ca²⁺-ATPase (SERCA), the L-type Ca²⁺-channel, the ryanodine receptor, the Na⁺/Ca²⁺ exchanger, or the Na⁺,K⁺-ATPase. Intracellular calcium levels were elevated significantly 8-24 hours postburn, and intracellular sodium was increased significantly 4 through 24 hours postburn. Expression of SERCA was significantly reduced 1-8 hours postburn while L-type Ca²⁺-channel expression was diminished 1 and 2 hours postburn (p<0.05), but returned toward control levels 4 hours postburn. Ryanodine receptor protein was significantly reduced at 1 and 2 hr postburn, returning to baseline by 4 hr postburn. Na⁺/Ca²⁺ exchanger expression was significantly elevated 2 hours postburn but was significantly reduced 24 hours postburn. An increase in Na⁺,K⁺-ATPase expression occurred 2-24 hours postburn. These data confirm that burn trauma alters calcium transporter expression, likely contributing to cardiomyocyte calcium loading and cardiac contractile dysfunction.