Regional sympathetic blockade unmasks potent vasodilation during hypoxia in sleep apnea

Abstract

Obstructive sleep apnea (OSA) is associated with excessive sympathetic activity, endothelial dysfunction and premature cardiovascular disease. To test the hypothesis that increased sympathetic activity in OSA might attenuate hypoxia-induced skeletal muscle vasodilation, we determined forearm blood flow (FBF, brachial artery) and vascular conductance (FVC) during systemic hypoxia (FiO2 0.1; 10 min) before and after regional sympathetic block in OSA (n=10) and weight- and age-matched controls (n=10). FBF was determined by ultrasound/Doppler and FVC was calculated as FBF/mean arterial pressure. Regional sympathetic block was achieved via Bier block with the α-receptor antagonist phentolamine. Pre phentolamine, during hypoxia (SaO2 79±1%), similar increases in FBF and FVC were noted in the 2 groups. Post phentolamine, the FBF and FVC responses to systemic hypoxia were markedly enhanced (control pre vs. post: 62±80 vs. 140±26 ml/min, P<0.01; and 0.58±0.07 vs. 1.30±0.24 units, P<0.01; OSA pre vs. post: 76±11 vs. 208±37 ml/min, P<0.002; and 0.71±0.11 vs. 1.83±0.31 units, P<0.002). However, following regional sympathetic block, FBF and FVC during hypoxia and the percent increase of FBF and FVC from baseline were not significantly different in the 2 groups (P=NS). We conclude that, despite the previously reported increased sympathetic activity in OSA, the ability to vasodilate during hypoxia is preserved, and, regional sympathetic block unmasks powerful vasodilator effects of hypoxia in OSA. This suggests that in OSA skeletal muscle metabolic vasodilator pathways may be up-regulated and act to offset the increased sympathetic vasoconstrictor nerve activity. Supported by R01 HL068699, P01 HL077670, M01 RR010732.