Sepsis and burn complicated by sepsis alter cardiac transporter expression

Abstract 

Sepsis alone and burn complicated by sepsis produce significant cardiac dysfunction. Since calcium handling by the cardiomyocyte is essential for cardiac function, one mechanism for cardiac abnormalities may be calcium dyshomeostasis. We hypothesized that sepsis and burn plus sepsis alter cardiac calcium transporter expression. Sprague-Dawley rats were divided into: (1) control, (2) sepsis (intratracheal S. Pneumoniae, 4×10⁶ CFU), and (3) burn (40% TBSA) plus sepsis. Myocyte [Ca²⁺]_i and [Na⁺]_i were quantified with Fura-2 AM and SBFI, respectively. Western blot analysis of rat hearts used antibodies against the sarcoplasmic reticular Ca²⁺ ATPase (SERCA), the L-type calcium channel, the Na⁺/Ca²⁺ exchanger or the Na⁺/K⁺ ATPase. RESULTS: Sepsis in the presence and absence of burn trauma increased [Ca²⁺]_i and [Na⁺]_i. SERCA expression was decreased in the sepsis and burn plus sepsis groups while calcium channel expression was transiently increased in these sepsis groups. Na⁺/Ca²⁺ exchanger expression exhibited a biphasic pattern of altered expression. Sepsis and burn plus sepsis reduced Na⁺/K⁺ ATPase protein levels. These data suggest that altered transporter expression produce cardiomyocyte calcium and sodium loading and may contribute to sepsis-mediated cardiac contractile dysfunction.

Keywords: SERCA, L-type calcium channels, Na, K-ATPase, Fluorescent indicators Fura 2AM and SBFI, Intratracheal Streptococcus pneumoniae, Rat model