Cutaneous burn trauma causes cardiac contraction and relaxation defects, but the mechanism is unclear. Previous studies suggest that burn-related changes in myocyte handling of calcium may play an important role in postburn cardiac dysfunction. With the use of a high dissociation constant (K_d) calcium indicator 1,2-bis(2-amino-5,6-difluorophenoxy)-ethane-N,N,N',N'-tetraacetic acid (TF-BAPTA) and ¹⁹F NMR spectroscopy, this study examined the correlation between the changes in cytosolic free calcium concentration ([Ca²⁺]_i) and cardiac function after burn trauma. Sprague-Dawley rats were given scald burn (over 40% of the total body surface area) or sham burn. Twenty-four hours later, the hearts were excised and perfused by the Langendorff method with a modified phosphate-free Krebs-Henseleit bicarbonate buffer. Left ventricular (LV) developed pressure (LVDP), calculated from peak systolic LV pressure and LV end-diastolic pressure, was assessed through a catheter attached to an intraventricular balloon. At the same time, ³¹P and ¹⁹F NMR spectroscopy was performed before and after TF-BAPTA loading. LVDP measured in hearts from burned rats was <40% than that measured in hearts from sham burn rats (65 ± 6 vs. 110 ± 12 mmHg, P < 0.01); [Ca²⁺]_i was increased fourfold in hearts from the burned group compared with that measured in the sham burn group (0.807 ± 0.192 vs. 3.891 ± 0.929 µM). Loading TF-BAPTA in hearts transiently decreased LVDP by 15%. Phosphocreatine-to-P_i ratio decreased, but ATP and intracellular pH remained unchanged by either TF-BAPTA loading or burn trauma. In conclusion, burn trauma impaired cardiac contractility, and this functional defect was paralleled by a significant rise in [Ca²⁺]_i in the heart.