Abstract

Abstract Introduction: A component of multiorgan dysfunction in burned patients is heart failure. Burn trauma has been shown to induce cytokine synthesis of IL-6, IL-1-beta, and TNF-alpha which can negatively impact cardiac function. We examined the effect of burn injury and lipopolysaccharide (LPS) exposure on cardiomyocyte contraction and cytokine secretion. Methods: Rats underwent a full-thickness 30%TBSA scald or sham burn. At 1,6,12 and 24 hours post-burn cardiomyocytes were isolated, plated at 50,000 cells/well, and incubated with 0, 1, 10, 25, and 50 micrograms/ml LPS for 18 hours. Supernatants were assayed by ELISA for IL-6, IL-1-beta, and TNF-alpha. Sarcomere length during contraction was recorded using a variable rate video camera with length detection software. Results: Peak relative sarcomere shortening was decreased in the burn vs. sham group at 1, 6, 12, and 24 hours post-burn (p Conclusions: Burn injury diminished peak sarcomere shortening. LPS inhibits sarcomere shortening in a dose-dependent fashion where cytokine levels are increased in cardiomyocytes 1 hour post-burn, this difference is abolished at 6, 12, and 24 hours. Exposure of cardiomyocytes to LPS does not have an effect on cytokine synthesis.

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