Proceedings of The Physiological Society

Europhysiology 2018 (London, UK) (2018) Proc Physiol Soc 41, PCB011

Poster Communications

Middle cerebral artery blood flow velocity regulation during short-term normobaric isocapnic hypoxia

S. alsalahi1, Y. Shang1, G. Balanos1, J. Fisher1

1. University of Birmingham, Birmingham, United Kingdom.

Hypoxia elicits ventilatory and cerebrovascular adjustments in order to defend against potential reductions in brain oxygenation. Hypoxia-mediated increases in cerebral blood flow can occur via local mechanism(s), but a secondary contribution may come from the elevated ventilation (e.g., augmented respiratory muscle pump and neurovascular coupling). We sought to isolate the contribution of hypoxia per se, from the possible secondary effect of increased ventilation, on increases in cerebral perfusion during short-term normobaric isocapnic hypoxia. In 11 young, healthy men (25±3 yr, mean±SD), middle cerebral artery mean blood flow velocity (MCAV; transcranial Doppler), mean arterial pressure (MAP; Finometer) and the partial pressure of end-tidal carbon dioxide (PETCO2) and oxygen (PETO2) were recorded. Cerebral vascular conductance index (CVCi) was calculated as MCAV / MAP. After a 10 min baseline, participants undertook four 10 min experimental trials during which PETO2 and PETCO2 were controlled using an end-tidal forcing system. The trials were; 1) normoxia [PETO2 = 100 mmHg], 2) hypoxia [PETO2 = 50 mmHg], 3) hypoxia with breathing frequency and tidal volume volitionally controlled at target levels measured during normoxia [PETO2 = 50 mmHg], and 4) normoxia with breathing voluntarily matched to target levels observed during hypoxia [PETO2 = 100 mmHg]. During all experimental trials, PETCO2 was held constantly to a baseline +1 mmHg level. Trials were separated by a rest period of ~20 min. Compared to normoxia (trial 1), during hypoxia (trial 2) increases were observed in ventilation (by ≈65%), MCAV (45±2 vs. 48±3 cm●s-1, mean±SE) and CVCi (0.84±0.05 vs. 0.95±0.05 mmHg/cm●s-1) (P<0.05). Hypoxia with controlled breathing (trial 3) also increased MCAV (52±3 cm●s-1) and CVCi (0.88±0.04 mmHg/cm●s-1) (P<0.05 vs. trial 1), while ventilation was not different to normoxic levels (P>0.05 vs. trial 1). During normoxia with controlled breathing (trial 4) ventilation was elevated as during hypoxia with spontaneous breathing (P<0.05 vs. trial 1), but MCAV (44±3 cm●s-1) and CVCi (0.81±0.05 mmHg/cm●s-1) were not different to that observed in normoxia with spontaneous breathing (P>0.05 vs. trial 1). In summary, at the level of isocapnic normobaric hypoxia studied, changes in blood oxygen concentration, and not a secondary effect of an increase in ventilation, make the predominate contribution to increases in cerebral perfusion.

Where applicable, experiments conform with Society ethical requirements