Abstract
Introduction. Severe burn trauma causes a catecholamine surge that has been demonstrated, in pediatric patients, to last up to 3 years post injury. The detrimental cardiac effects of the catecholamine surge include a reduction of functional β‐adrenergic receptors (β‐AR) and alterations in various signaling pathways such as that of extracellular signal regulated kinase (Erk1/2).Methods. We used a rat model of 60% total body surface area burn to investigate burn‐induced changes in cardiac signaling pathways. Animals were sacrificed and hearts were isolated 24 hrs and 7 days post injury. The expression and phosphorylation of proteins involved in Erk1/2 signaling were examined via Western Blot.Results. β1‐AR expression levels were significantly increased 24 hrs post‐burn (p=0.009) but returned to control levels by 7 days post‐burn. No changes were observed in β2‐AR expression levels. Gi expression was initially depressed post‐burn but was increased at 7 days post‐burn (p=0.0009). Similarly, Erk1/2 phosphorylation was increased by 7 days post‐burn (p=0.036). However, Akt phosphorylation was decreased at 7 days post‐burn (p=0.01).Conclusion. These data indicate that burn injury alters Erk1/2 activation and activity, which may promote pro‐hypertrophic and pro‐apoptotic signaling. Furthermore, in the long‐term, these changes may underlie burn induced cardiac dysfunction and subsequent mortality.Grant Funding Source: Supported by grants from the NIH (P50‐GM60338, KL2RR029875,UL1RR029876) and SHC (80100, 71001).
Published Version
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