We have shown previously that
burn trauma produces significant cardiac dysfunction, which is first evident 8 h postburn and is maximal 24 h postburn. Because
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 by fura 2-AM or
sodium-binding benzofuran isophthalate fluorescent indicators, respectively. In addition, hearts freeze-clamped at various times postburn (2, 4, 8, and 24 h) were used for Western blot analysis using
antibodies against the
sarcoplasmic reticulum calcium-ATPase (SERCA), the
L-type calcium-channel, the
ryanodine receptor, the
sodium/calcium exchanger, or the
sodium-potassium-ATPase. Intracellular
calcium levels were elevated significantly 8-24 h postburn, and intracellular
sodium was increased significantly 4 through 24 h postburn. Expression of SERCA was significantly reduced 1-8 h postburn, whereas
L-type calcium-channel expression was diminished 1 and 2 h postburn (P < 0.05) but returned toward control levels 4 h postburn.
Ryanodine receptor protein was significantly reduced at 1 and 2 h postburn, returning to baseline by 4 h postburn.
Sodium/calcium exchanger expression was significantly elevated 2 h postburn but was significantly reduced 24 h postburn. An increase in
sodium-potassium-ATPase expression occurred 2-24 h postburn. These data confirm that
burn trauma alters
calcium transporter expression, likely contributing to cardiomyocyte
calcium loading and cardiac contractile dysfunction.