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Assessment of Vascular Function in Patients With Chronic Kidney Disease
Published on: June 16, 2014
No effect of fitness on brachial or forearm vascular function during acute inflammation in young adults
Elizabeth C Schroeder1, Thessa I M Hilgenkamp1, Wesley K Lefferts1
1Integrative Physiology Laboratory, Department of Kinesiology and Nutrition, University of Illinois at Chicago, Chicago, Illinois.
Abstract:
Acute inflammation is associated with increased risk of cardiovascular events and impaired vasodilatory capacity. Vasodilatory capacity can be measured in different segments of the arterial tree; however, it is unknown if the effects of acute inflammation are vascular segment-specific or if inflammation-induced dysfunction can be attenuated by factors that modulate cardiovascular risk, such as high cardiorespiratory fitness. The purpose of this study was to determine the effect of acute inflammation and fitness on conduit artery, resistance artery, and microvascular function in healthy, young adults. Vascular function was assessed at baseline and 24 h after a typhoid vaccination in 11 low-fit (5 male, 24 yr of age, 34.5 ± 2.9 ml·kg-1·min-1 peak O2 uptake (V̇o2peak)] and 12 high-fit (7 male, 27 yr of age, 56.4 ± 9.7 ml·kg-1·min-1 V̇o2peak) young adults. Vascular assessments included flow-mediated dilation (FMD) of the brachial artery, forearm reactive hyperemia (RH) via venous occlusion plethysmography, and near-infrared spectroscopy (NIRS) during a 5-min arterial occlusion. Acute inflammation was evident with increases in IL-6 and C-reactive protein (P < 0.01), and mean arterial pressure did not change (P = 0.33). FMD was lower in the high-fit group, yet it was reduced in both groups at 24 h, even after controlling for shear (P < 0.05). No effect of acute inflammation was observed for RH or NIRS (P > 0.05). Acute inflammation had nonuniform effects on vascular function throughout the arterial tree in young adults, and fitness did not alter the vascular response. This suggests that cardiorespiratory fitness may not protect the vasculature during acute inflammation in young adults in the absence of age- or disease-related decline in vascular function.
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