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The impact of severe burn injury on cardiac mitochondrial function

Hypermetabolism, hypercatabolism, inflammation, and muscle wasting are all key characteristics of the pathophysiological response to severe burn injury. Severe burn injury also induces an exaggerated and prolonged release of catecholamines. These catecholamines include norepinephrine and epinephrine, which activate β‐adrenergic receptors (β‐ARs). The over‐activation of β‐ARs leads to increased resting heart rate and cardiac work, which is associated with morbidity and increased risk of mortality. We have previously shown that severe burn injury causes mitochondrial dysfunction in skeletal muscle, which persists for more than a year after injury. We hypothesized that cardiac mitochondrial function would also be altered by burn injury.