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Published on: February 3, 2017
Cardiomyocyte function after burn injury and lipopolysaccharide exposure: single-cell contraction analysis and
Andreas D Niederbichler1, Margaret V Westfall, Grace L Su
1Department of Surgery, University of Michigan Medical School, Ann Arbor, MI 48109, USA.
Insights
Burn injury and lipopolysaccharide (LPS) exposure independently impair heart cell contraction. Cytokine levels initially increased post-burn but did not correlate with reduced cardiac function from LPS or burn trauma.
Area of Science:
- Cardiovascular Physiology
- Burn Trauma Research
- Immunology
Background:
- Heart failure is a key component of multiorgan dysfunction in burn patients.
- Burn trauma triggers inflammatory cytokine release (IL-1β, IL-6, TNF-α), potentially impairing cardiac function.
- Infectious complications are frequent after severe burns, often involving endotoxins like lipopolysaccharide (LPS).
Purpose of the Study:
- To investigate the independent and combined effects of burn injury and lipopolysaccharide (LPS) exposure on cardiomyocyte contractility.
- To determine the impact of burn injury and LPS on the secretion of key inflammatory cytokines (IL-1β, IL-6, TNF-α) by cardiomyocytes.
Main Methods:
- Rats underwent a 30% total body surface area scald burn or sham procedure.
- Cardiomyocytes were isolated at various time points (1, 6, 12, 24 hours post-burn) and exposed to increasing doses of LPS.
- Peak sarcomere shortening and contractile velocity were measured; cytokine levels in supernatants were quantified using ELISA.
Main Results:
- Burn injury significantly decreased peak cardiomyocyte sarcomere shortening at all measured time points.
- LPS exposure caused a dose-dependent reduction in sarcomere shortening in both sham and burned animals.
- While burn injury initially increased cardiomyocyte cytokine levels (IL-1β, IL-6, TNF-α), LPS exposure did not elevate cytokine secretion but exacerbated the contractile dysfunction.
Conclusions:
- Both burn injury and LPS exposure independently impair cardiomyocyte peak shortening.
- The observed decreases in cardiac contractility did not directly correlate with the measured cytokine levels.
- These findings highlight distinct mechanisms by which burn trauma and LPS contribute to cardiac dysfunction.
Abstract:
A component of multiorgan dysfunction in burned patients is heart failure. Burn trauma induces cytokine synthesis of interleukin (IL) 1beta, IL-6, and tumor necrosis factor alpha (TNF-alpha) which can negatively impact cardiac function. Infectious complications are common following severe burn injury. We hypothesized that burn injury and lipopolysaccharide (LPS) exposure independently influence peak cardiomyocyte contraction and cytokine secretion. Rats underwent a full-thickness 30% total body surface area scald or sham burn. At 1, 6, 12, and 24 h after burn, cardiomyocytes were isolated and incubated with increasing LPS doses. Peak sarcomere shortening and contractile velocity parameters were recorded using a variable-rate video camera with sarcomere length detection software. Supernatants were assayed for IL-1beta, IL-6, and TNF-alpha by ELISA. Peak sarcomere shortening was decreased in the burn group at 1, 6, 12, and 24 h after burn. IL-1beta, IL-6, and TNF-alpha levels were increased in cardiomyocytes isolated 1 h after burn compared with sham controls, but returned to sham levels at 6, 12, and 24 h after burn. LPS exposure caused dose-dependent decreases in sarcomere shortening in sham and burn animals. LPS exposure did not produce increased cardiomyocyte cytokine expression. Burn injury diminished peak sarcomere shortening. Whereas exposure to LPS did not have an effect on cardiomyocyte cytokine expression, LPS significantly inhibited sarcomere shortening in a dose-dependent fashion. Combined burn and LPS exposure inhibited sarcomere shortening more than each alone. These results demonstrate that LPS exposure and burn injury independently decrease peak cardiac shortening. These decreases did not directly correlate with the levels of cytokines released in response to each stressor.
