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. 2018 Nov 1;315(5):R1054-R1060.
doi: 10.1152/ajpregu.00188.2018. Epub 2018 Sep 26.

Vasodilator function is impaired in burn injury survivors

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Vasodilator function is impaired in burn injury survivors

Steven A Romero et al. Am J Physiol Regul Integr Comp Physiol. .

Abstract

The effect of severe burn injury on vascular health is unknown. We tested the hypothesis that, compared with nonburn control subjects, vasodilator function would be reduced and that pulse-wave velocity (a measure of arterial stiffness) would be increased in individuals with prior burn injuries, the extent of which would be associated with the magnitude of body surface area having sustained a severe burn. Pulse-wave velocity and macrovascular (flow-mediated dilation) and microvascular (reactive hyperemia) dilator functions were assessed in 14 nonburned control subjects and 32 age-matched subjects with well-healed burn injuries. Fifteen subjects with burn injuries covering 17-40% of body surface area were assigned to a moderate burn injury group, and 17 subjects with burn injuries covering >40% of body surface area were assigned to a high burn injury group. Pulse-wave velocity [ P = 0.3 (central) and P = 0.3 (peripheral)] did not differ between the three groups. Macrovascular dilator function was reduced in the moderate ( P = 0.07) and high ( P < 0.05) burn injury groups compared with the control group. Likewise, peak vascular conductance during postocclusive reactive hyperemia differed from the moderate burn injury group ( P = 0.08 vs. control) and the high burn injury group ( P < 0.05 vs. control). These data suggest that vasodilator function is impaired in well-healed burn injury survivors, with the extent of impairment not dependent on the magnitude of body surface area having sustained a severe burn injury.

Keywords: burn injury; flow-mediated dilation; reactive hyperemia.

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Figures

Fig. 1.
Fig. 1.
Endothelium-dependent macrovascular dilator function as assessed by analysis of covariance adjusted flow-mediated dilation (A) and endothelium-independent dilation assessed via glyceryl trinitrate (GTN)-mediated dilation (B). *P < 0.05 vs. control; †P = 0.07 vs. control.
Fig. 2.
Fig. 2.
Microvascular dilator function as assessed by peak vascular conductance (A) and area under the curve (B) during postreactive hyperemia. *P < 0.05 vs. control; †P = 0.08 vs. control.

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