Sympathoadrenal Modulation of Stress-Activated Signaling in Burn Trauma

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Abstract
Burn injury stimulates stress-responsive components, p38 mitogen-activated protein kinase (MAPK)/c-Jun N-terminal kinases (JNK)/nuclear factor (NF)-κB. p38 MAPK plays a role in postburn cardiomyocyte tumor necrosis factor-α secretion and cardiac dysfunction. Since burn trauma increases circulating catecholamine levels, which in turn modulate inflammatory cytokine production, we hypothesized that increased sympathetic activity after major burn trauma may trigger postburn cardiac p38 MAPK activation via an adrenergic receptor-mediated phenomenon. We examined adrenergic receptor populations involved in burn-activated cardiac stress signaling. Sprague Dawley rats were divided into six groups: 1) control, 2) control plus α1-adrenergic agonist phenylephrine (2 μg/kg, intravenous), 3) control plus β-adrenergic agonist isoproterenol (1 μg/kg, intravenous), 4) burn (fluid resuscitation with lactated Ringer's 4 ml/kg/% burn), 5) burn plus α1-adrenergic antagonist prazosin (1 mg/kg, by mouth), and 6) burn plus β-adrenergic antagonist propranolol (3.3 mg/kg, by mouth). Phenylephrine, but not isoproterenol, increased cardiac p38 MAPK/JNK/NF-κB activation. Burn trauma activated p38 MAPK, JNK, and NF-κB, and this stress response was blocked by either prazosin or propranolol. Thus, stimulation of the adrenergic pathway may constitute one upstream activator of stress response in burn.

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