4.3 Article

The middle cerebral artery blood velocity response to acute normobaric hypoxia occurs independently of changes in ventilation in humans

期刊

EXPERIMENTAL PHYSIOLOGY
卷 106, 期 4, 页码 861-867

出版社

WILEY
DOI: 10.1113/EP089127

关键词

blood flow; brain; heart rate; ventilation

资金

  1. Kuwait Government

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This study investigated the impact of ventilatory response on cerebral perfusion during moderate isocapnic acute hypoxia in humans. The findings suggest that the ventilatory response does not increase cerebral perfusion beyond the changes induced by reduced oxygen saturation, indicating that the body's natural responses to hypoxia adequately regulate cerebral blood flow.
New Findings What is the central question of this study? Does the ventilatory response to moderate acute hypoxia increase cerebral perfusion independently of changes in arterial oxygen tension in humans? What is the main finding and its importance? The ventilatory response does not increase middle cerebral artery mean blood velocity during moderate isocapnic acute hypoxia beyond that elicited by reduced oxygen saturation. Hypoxia induces ventilatory, cardiovascular and cerebrovascular adjustments to defend against reductions in systemic oxygen delivery. We aimed to determine whether the ventilatory response to moderate acute hypoxia increases cerebral perfusion independently of changes in arterial oxygenation. Eleven young healthy individuals were exposed to four 15 min experimental conditions: (1) normoxia (partial pressure of end-tidal oxygen, PETO2 = 100 mmHg), (2) hypoxia (PETO2 = 50 mmHg), (3) normoxia with breathing volitionally matched to levels observed during hypoxia (hyperpnoea; PETO2 = 100 mmHg) and (4) hypoxia (PETO2( )= 50 mmHg) with respiratory frequency and tidal volume volitionally matched to levels observed during normoxia (i.e., restricted breathing (RB)). Isocapnia was maintained in all conditions. Middle cerebral artery mean blood velocity (MCA V-mean), assessed by transcranial Doppler ultrasound, was increased during hypoxia (58 +/- 12 cm/s, P = 0.04) and hypoxia + RB (61 +/- 14 cm/s, P < 0.001) compared to normoxia (55 +/- 11 cm/s), while it was unchanged during hyperpnoea (52 +/- 13 cm/s, P = 0.08). MCA V-mean was not different between hypoxia and hypoxia + RB (P > 0.05). These findings suggest that the hypoxic ventilatory response does not increase cerebral perfusion, indexed using MCA V-mean, during moderate isocapnic acute hypoxia beyond that elicited by reduced oxygen saturation.

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