Cerebrovascular response to the cold pressor test – the critical role of carbon dioxide

Abstract

In addition to increasing sympathetic nervous activity, blood pressure, and cerebral blood flow (CBF), the cold pressor test (CPT) stimulates pain receptors, which may increase ventilation above metabolic demand; this response likely reduces the partial pressure of end-tidal carbon dioxide (P_ETCO₂), and will attenuate elevations in CBF. We hypothesized: (1) CPT would elicit hyperventilation, effectively lowering P_ETCO₂; (2) the CBF response will be elevated during an isocapnic (controlled P_ETCO₂), compared to a poikilocapnic CPT (uncontrolled P_ETCO₂); (3) In response to CPT, the common carotid artery (CCA) will vasodilatate, while the internal carotid artery (ICA) will remain unchanged to help regulate CBF. Using a novel, randomized experimental design, we measured the cerebrovascular response in the middle cerebral artery (MCA), CCA, and ICA, during an isocapnic and poikilocapnic CPT in 15 participants. Blood pressure and cardiac output (finger photoplethysmography), heart rate (electrocardiogram), MCA mean velocity (transcranial Doppler ultrasound), and CCA and ICA CBF (Duplex ultrasound) were recorded during both CPT trials. Our findings were: (1) ventilation increased, which reduced P_ETCO₂ (−5.3 ± 6.4 mmHg) during the poikilocapnic, compared to the isocapnic CPT; (2) the CBF response was elevated during the isocapnic compared to the poikilocapnic CPT in the MCA and ICA, but not in the CCA; (3) The CCA dilated to a greater extent during the isocapnic, compared to poikilocapnic CPT, and the ICA vasocontricted during both trials. Our data emphasizes the importance of P_ETCO₂ control in the CBF response to CPT and in the differential vasomotor regulation between the CCA and ICA.

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