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 (19)F NMR spectroscopy, this study examined the correlation between the changes in cytosolic free
calcium concentration ([Ca(2+)](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, (31)P and (19)F 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); [Ca(2+)](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 microM). 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 [Ca(2+)](i) in the heart.