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Sepsis and burn complicated by sepsis alter cardiac transporter expression
Cherry Ballard-Croft1, David L Maass, Patricia J Sikes
1Department of Surgery, University of Kentucky, Lexington, Kentucky, USA.
Insights
Sepsis and burn injuries disrupt heart function by altering cardiomyocyte calcium and sodium levels. This study reveals changes in key calcium transporters, potentially explaining sepsis-induced cardiac dysfunction.
Area of Science:
- Cardiology
- Molecular Biology
- Physiology
Background:
- Sepsis and burn injuries can lead to significant cardiac dysfunction.
- Proper cardiomyocyte calcium handling is crucial for maintaining cardiac function.
- Calcium dyshomeostasis is a potential mechanism underlying sepsis-related cardiac abnormalities.
Purpose of the Study:
- To investigate the hypothesis that sepsis and burn trauma alter cardiac calcium transporter expression.
- To quantify intracellular calcium ([Ca(2+)](i)) and sodium ([Na(+)](i)) levels in cardiomyocytes.
- To analyze the expression of key cardiac ion transporters.
Main Methods:
- Utilized Sprague-Dawley rats divided into control, sepsis, and burn plus sepsis groups.
- Quantified myocyte intracellular calcium and sodium using Fura-2 AM and SBFI indicators.
- Performed Western blot analysis to assess the expression of sarcoplasmic reticular Ca(2+) ATPase (SERCA), L-type calcium channel, Na(+)/Ca(2+) exchanger, and Na(+)/K(+) ATPase.
Main Results:
- Sepsis, with or without burn trauma, increased intracellular calcium and sodium levels.
- SERCA expression decreased, while calcium channel expression was transiently increased in sepsis groups.
- Na(+)/K(+) ATPase protein levels were reduced, and Na(+)/Ca(2+) exchanger expression showed a biphasic alteration.
Conclusions:
- Altered expression of cardiac transporters contributes to cardiomyocyte calcium and sodium loading during sepsis.
- These transporter changes may play a role in the cardiac contractile dysfunction observed in sepsis.
- Findings suggest a molecular basis for sepsis-induced heart dysfunction involving ion transport disruption.
Unlabelled:
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, 4x10(6) CFU), and (3) burn (40% TBSA) plus sepsis. Myocyte [Ca(2+)](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 Ca(2+) ATPase (SERCA), the L-type calcium channel, the Na(+)/Ca(2+) exchanger or the Na(+)/K(+) ATPase.
Results:
Sepsis in the presence and absence of burn trauma increased [Ca(2+)](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(+)/Ca(2+) 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.
