The Effect of an Antioxidant Cocktail on Endothelial Function in Healthy Caucasian and African American Men

Abstract

African Americans (AA) have elevated risk of developing a variety of cardiovascular and metabolic diseases relative to Caucasian Americans (CA). The reason for this elevated disease risk in the AA population is multifactorial with impaired vascular function being a key contributing factor. The exact mechanism(s) leading to vascular dysfunction in AA are not well understood; however, elevated oxidative stress is likely a factor. We have recently demonstrated that local administration of the superoxide dismutase mimetic Tempol improves endothelial function in the cutaneous microvasculature of AA. However, the systemic effects of antioxidants on indices of vascular function are not well characterized in this population. Therefore, the purpose of the current investigation was to test the hypothesis that an antioxidant cocktail (AOX), previously shown to decrease superoxide production in young, healthy men, will acutely augment endothelial function in AA as determined by flow mediated dilation (FMD). Four healthy, college‐aged AA men and 3 age‐matched CA men were studied on two mornings after an overnight fast separated by ~1 week. Upon arrival to the lab, either AOX (vitamin C: 2g, vitamin E: 150IU, and coenzyme Q10: 100mg) or a placebo (three sugar pills) was given in a randomized order. 120min after treatment, following a 2 min baseline a cuff placed 3cm distal to the elbow was inflated to 220 mmHg for 5 min and then rapidly deflated. Post‐occlusion data was collected for an additional 3 min. Brachial artery diameter and blood velocity were continuously assessed via duplex Doppler ultrasound. AOX had no effect on FMD in either group (AA Placebo: 6.6 ± 2.1; AA AOX: 5.9 ±1.7; CA Placebo: 3.6 ± 1, CA AOX: 5.0 ± 1.5% FMD, P=0.32). This result remained when FMD was corrected for hyperemic shear rate area under the curve (AUC) (P=0.11). In contrast, the hyperemic velocity AUC was augmented by AOX in the AA (Placebo: 1014.7 ± 537, AOX: 1944 ± 564 a.u., P=0.03) but not in the CA (Placebo: 1781.3 ± 362, AOX: 1468.1 ± 644 a.u., P=0.54) suggesting AOX improves microvascular reactivity in AA. Collectively, these preliminary findings suggest that AOX does not affect conduit artery endothelial function in AA or CA as assessed by FMD. However, AOX augments microvascular function in skeletal muscle of AA. These data are consistent with our previous findings suggesting oxidative stress attenuates microvascular function in healthy, young AA.