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UBC Theses and Dissertations

The effects of intermittent hypoxia on the vasculature and the carotid baroreflex regulation of arterial pressure Tremblay, Joshua Christopher


Intermittent hypoxia (IH) occurs in association with obstructive sleep apnea and is thought to contribute to the pathogenesis of hypertension. The proposed mechanisms involved include endothelial dysfunction, arterial stiffness, increased vascular resistance and impaired arterial baroreflex. We sought to examine the effects of a single 6-hour bout of IH on the global vascular, and carotid baroreflex regulation of mean arterial pressure (MAP). We hypothesized that 6 hours of IH would increase 24-hour MAP, reduce endothelium-dependent vasodilation, impair vascular strain, induce oscillatory conduit artery shear patterns and shift the carotid baroreflex to operate at higher MAP while eliciting blunted control of leg vascular conductance (LVC). Ten young, normotensive men free of sleep apnea were exposed to two 6-hour conditions: 1) breathing one-minute of room air followed by one-minute of hypoxia (IH; mean minimum oxygen saturation = 80.7±0.4% [mean±SEM]), and 2) breathing room air (SHAM). Arterial blood pressure was recorded using 24-hour ambulatory blood pressure monitoring. Brachial artery flow-mediated dilation and reactive hyperemia were measured before and immediately after each condition 6-hour protocol. Vascular strain was measured using two-dimensional speckle-tracking in the common carotid and femoral artery, in addition to upper and lower limb hemodynamics during each testing condition. Carotid baroreflex control of MAP and LVC was assessed after each testing condition using the variable pressure neck chamber technique. Six hours of IH elevated 24-hour MAP (2.6±0.8 mmHg, P=0.008). Reactive hyperemia and flow-mediated dilation were unaffected by IH. Common carotid artery strain was reduced during IH compared to SHAM (room air cycle, P=0.012; hypoxia cycle, P<0.001) and a trend towards IH-impaired common femoral artery strain was observed (P=0.055). The lower limb exhibited enhanced oscillatory shear only during IH. Intermittent hypoxia displaced the carotid baroreflex control of MAP curve to higher arterial blood pressures (P=0.045) and blunted LVC responses to hypertensive stimuli. Oscillatory shear patterns in the lower limbs, impaired vascular strain and blunted carotid baroreflex control of LVC may be involved in IH-induced hypertension, providing insight on the early pathogenic processes.

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