Abstract
Severe burns result in cardiovascular dysfunction, but responses in the peripheral vasculature are unclear. We hypothesize that severe burns disturb arterial contractility through acute changes in adrenergic and cholinergic receptor function. To address this, we investigated the changes in carotid artery contractility and relaxation following a severe burn. Thirty-four adult Sprague–Dawley male rats received a 40% total body surface area (TBSA) scald burn and fluid resuscitation using the Parkland formula. Control animals received sham burn procedure. Animals were serially euthanized between 6 h and 14 days after burn and endothelium-intact common carotid arteries were used for ex vivo force/relaxation measurements. At 6 h after burn, carotid arteries from burned animals demonstrated a > 50% decrease in cumulative dose-responses to norepinephrine (p < 0.05) and to 10−7 M angiotensin II (p < 0.05). Notably, pre-constricted carotid arteries also demonstrated reduced relaxation responses to acetylcholine (p < 0.05) 6 h after burn, but not to sodium nitroprusside. Histologic examination of cross-sectional planes revealed significant increases in carotid artery wall thickness in burned rats at 6 h versus 3 days, with increased collagen expression in tunica media at 3 days (p < 0.05). Carotid artery dysfunction occurs within 6 h after severe burn, demonstrating decreased sensitivity to adrenergic- and angiotensin II-induced vasoconstriction and acetylcholine-induced relaxation.
Highlights
Severe burns result in cardiovascular dysfunction, but responses in the peripheral vasculature are unclear
Vasoconstriction is induced by changes in C a2+, adenosine triphosphate (ATP), α1-adrenergic receptor agonists and angiotensin II (AngII) through activation of vascular smooth muscle (VSM) specific receptors and ion c hannels[9]
We report for the first time the dynamic changes that occur in carotid artery function following severe burn
Summary
Severe burns result in cardiovascular dysfunction, but responses in the peripheral vasculature are unclear. We investigated the changes in carotid artery contractility and relaxation following a severe burn. Carotid artery dysfunction occurs within 6 h after severe burn, demonstrating decreased sensitivity to adrenergicand angiotensin II-induced vasoconstriction and acetylcholine-induced relaxation. Along with other vasoactive mediators, serum epinephrine is dramatically increased in trauma patients within 4 h from injury[6] These responses, when prolonged, lead to complications such as cardiac dysfunction and delayed wound h ealing[7]. What effect these changes have on peripheral arterial function is not known. We posit that severe burns alter peripheral arterial vascular contractility by modifying adrenergic and cholinergic receptor-mediated smooth muscle contraction. We report for the first time the dynamic changes that occur in carotid artery function following severe burn
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