Effect of acute hypoxia on regional cerebral blood flow: effect of sympathetic nerve activity

Abstract

We examined 1) whether global cerebral blood flow (CBF) would increase across a 6-h bout of normobaric poikilocapnic hypoxia and be mediated by a larger increase in blood flow in the vertebral artery (VA) than in the internal carotid artery (ICA); and 2) whether additional increases in global CBF would be evident following an α1-adrenergic blockade via further dilation of the ICA and VA. In 11 young normotensive individuals, ultrasound measures of ICA and VA flow were obtained in normoxia (baseline) and following 60, 210, and 330 min of hypoxia (FiO2 = 0.11). Ninety minutes prior to final assessment, participants received an α1-adrenoreceptor blocker (prazosin, 1 mg/20 kg body mass) or placebo. Compared with baseline, following 60, 220, and 330 min of hypoxia, global CBF [(ICAFlow + VAFlow) ∗ 2] increased by 160 ± 52 ml/min (+28%; P = 0.05), 134 ± 23 ml/min (+23%; P = 0.02), and 113 ± 51 (+19%; P = 0.27), respectively. Compared with baseline, ICAFlow increased by 23% following 60 min of hypoxia (P = 0.06), after which it progressively declined. The percentage increase in VA flow was consistently larger than ICA flow during hypoxia by ∼20% (P = 0.002). Compared with baseline, ICA and VA diameters increased during hypoxia by ∼9% and ∼12%, respectively (P ≤ 0.05), and were correlated with reductions in SaO2. Flow and diameters were unaltered following α1 blockade (P ≥ 0.10). In conclusion, elevations in global CBF during acute hypoxia are partly mediated via greater increases in VA flow compared with ICA flow; this regional difference was unaltered following α1 blockade, indicating that a heightened sympathetic nerve activity with hypoxia does not constrain further dilation of larger extracranial blood vessels.

Indomethacin‐induced impairment of regional cerebrovascular reactivity: implications for respiratory control

“…; Lewis et al . ) that reported higher relative CVR in the VA compared to ICA (based on n = 11), we report no difference in CVR ( n = 11). This disparity is likely to be due to differing characteristics of both the hypoxic exposure and calculation of reactivity.…”

“…; Lewis et al . ) highlight the need to utilize both posterior and volumetric blood flow measures when investigating the relationship between CVR and ventilation. The mechanism by which increased reactivity increases the magnitude of HVD in humans is somewhat speculative.…”

Unexpected reductions in regional cerebral perfusion during prolonged hypoxia

“…; Lewis et al . ; Lawley et al . a ), especially if is maintained via end‐tidal clamping procedures (Willie et al .…”

Regulation of Brain Blood Flow and Oxygen Delivery in Elite Breath-Hold Divers

“…6,7 Data on CBF in humans are generally in the context of either hypobaric hypoxia, i.e., high altitude 5,[8][9][10][11] or by various means of altering inspired gases to induce acute poikilocapnic or isocapnic hypoxia. 6,7,12 Elite breath-hold divers experience a similar or greater magnitude of transient hypoxemia as do individuals exposed to very high altitudes, but with concomitant acidosis due to build up of blood and tissue CO 2 . Prolonged apnea thus features two factors (hypoxia and hypercapnia) that together generate an extremely potent cerebral vasodilatory stimulus.…”