Effect of acute hypoxia on blood flow in vertebral and internal carotid arteries

<jats:title>New Findings</jats:title><jats:p><jats:list list-type="explicit-label"> <jats:list-item><jats:p><jats:bold>What is the central question of this study?</jats:bold></jats:p><jats:p>Does hypoxia enhance blood flow to all parts of the brain uniformly?</jats:p></jats:list-item> <jats:list-item><jats:p><jats:bold>What is the main finding and its importance?</jats:bold></jats:p><jats:p>During hypoxia, internal carotid artery flow is maintained despite a reduction in (end‐tidal) carbon dioxide tension, while vertebral artery blood flow increases. Only with maintained end‐tidal carbon dioxide tension is there an increase in both vertebral and internal carotid blood flow during hypoxia.</jats:p></jats:list-item> </jats:list></jats:p><jats:p>Hypoxia changes the regional distribution of cerebral blood flow and stimulates the ventilatory chemoreflex, thereby reducing CO<jats:sub>2</jats:sub> tension. We examined the effects of both hypoxia and isocapnic hypoxia on acute changes in internal carotid (ICA) and vertebral artery (VA) blood flow. Ten healthy male subjects underwent the following two randomly assigned respiratory interventions after a resting baseline period with room air: (i) hypoxia; and (ii) isocapnic hypoxia with a controlled gas mixture (12% O<jats:sub>2</jats:sub>; inspiratory <jats:inline-graphic xmlns:xlink="http://www.w3.org/1999/xlink" xlink:href="graphic/EPH_1235_mu1.gif" xlink:title="inline image" /> mmHg). In the isocapnic hypoxia intervention, subjects were instructed to maintain the rate and depth of breathing to maintain the level of end‐tidal partial pressure of CO<jats:sub>2</jats:sub> (<jats:inline-graphic xmlns:xlink="http://www.w3.org/1999/xlink" xlink:href="graphic/EPH_1235_mu2.gif" xlink:title="inline image" />) during the resting baseline period. The ICA and VA blood flow (velocity × cross‐sectional area) were measured using Doppler ultrasonography. The <jats:inline-graphic xmlns:xlink="http://www.w3.org/1999/xlink" xlink:href="graphic/EPH_1235_mu3.gif" xlink:title="inline image" /> was decreased (−6.3 ± 0.9%, <jats:italic>P</jats:italic> < 0.001) during hypoxia by hyperventilation (minute ventilation +12.9 ± 2.2%, <jats:italic>P</jats:italic> < 0.001), while <jats:inline-graphic xmlns:xlink="http://www.w3.org/1999/xlink" xlink:href="graphic/EPH_1235_mu4.gif" xlink:title="inline image" /> was unchanged during isocapnic hypoxia. The ICA blood flow was unchanged (<jats:italic>P</jats:italic>= 0.429), while VA blood flow increased (+10.3 ± 3.1%, <jats:italic>P</jats:italic>= 0.010) during hypoxia. In contrast, isocapnic hypoxia increased both ICA (+14.5 ± 1.4%, <jats:italic>P</jats:italic> < 0.001) and VA blood flows (+10.9 ± 2.4%, <jats:italic>P</jats:italic> < 0.001). Thus, hypoxic vasodilatation outweighed hypocapnic vasoconstriction in the VA, but not in the ICA. These findings suggest that acute hypoxia elicits an increase in posterior cerebral blood flow, possibly to maintain essential homeostatic functions of the brainstem.</jats:p>