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Ventilatory, cerebrovascular, and cardiovascular interactions in acute hypoxia: regulation by carbon dioxide

Departments of ¹Physiology and Biophysics and ²Clinical Neurosciences, Faculty of Medicine, and ³Faculty of Kinesiology, University of Calgary, Calgary, Alberta, Canada T2N 4N1

Submitted 22 December 2003 ; accepted in final form 1 March 2004

This study examined the effect of high, normal, and uncontrolled end-tidal PCO₂ (PET_CO2) on the ventilatory, peak cerebral blood flow velocity (_p), and mean arterial blood pressure (MAP) responses to acute hypoxia. Nine healthy subjects undertook, in random order, three hypoxic protocols (end-tidal PO₂ was held at eight steps between 300 and 45 Torr) in conditions of hypercapnia, isocapnia, or poikilocapnia (PET_CO2 +7.5 Torr, +1.0 Torr, or uncontrolled, respectively). Transcranial Doppler ultrasound was used to measure _p in the middle cerebral artery. The slopes of the linear regressions of ventilation, _p, and MAP with arterial O₂ saturation were significantly greater in hypercapnia than in both isocapnia and poikilocapnia (P < 0.05). Strong, significant correlations were observed between ventilation, _p, and MAP with each PET_CO2 condition. These data suggest that 1) a high acute hypoxic ventilatory response (AHVR) decreases the acute hypoxic cerebral blood flow responses during poikilocapnia hypoxia, due to hypocapnic-induced cerebral vasoconstriction; and 2) in hypercapnic hypoxia, a high AHVR is associated with a high acute hypoxic cerebral blood flow response, demonstrating a linkage of individual sensitivities of ventilation and cerebral blood flow to the interaction of PET_CO2 and hypoxia. In summary, the between-individual variability in AHVR is shown to be firmly linked to the variability in _p and MAP responses to hypoxia. Individuals with a high AHVR are found also to have high _p and MAP responses to hypoxia.

cerebral blood flow; ventilation; hypercapnia; isocapnia; poikilocapnia

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