Author(s): MCCRONE, J.C.1, OSEI-BOATENG, C.1, MINERS, N.I.1, ROY, M.A.2, MACLEOD, D.B.3, AMARAL, S.3, GABRIELYAN, G.4, MAIER, L.E.5, TSIOROS, S.L.1, THIESSEN, J.S.1, FERNANDES, I.A.6, SMITH, K.J.7, BAIN, A.R.8, GASHO, C.J.4, STACEY, B.S.9, TYMKO, M.M.1, Institution: UNIVERSITY OF GUELPH, Country: CANADA, Abstract-ID: 2669

INTRODUCTION:
Despite well-established mechanisms that govern cerebral blood flow (CBF) and ventilation (V̇E), the contribution of sympathetic nerve activity (SNA) remains poorly characterized, particularly at high-altitude. We hypothesized that reducing regional SNA at sea-level and high-altitude via unilateral stellate ganglion blockade (SGB) would increase CBF at rest and augment cerebrovascular and ventilatory reactivity to hypercapnia and hypoxia, without altering cardiovascular variables.
METHODS:
Seven healthy participants (1F; 32±7yrs) underwent cardiorespiratory and cerebrovascular monitoring at sea-level (334m) and high-altitude (3,800m) on days 3-5 following ascent. Participants were equipped with measures of heart rate (three-lead electrocardiogram in lead II orientation), blood pressure (finger photoplethysmography), and peripheral oxygen saturation, with V̇E and end-tidal gases controlled through dynamic end-tidal forcing. Bilateral measures of internal carotid artery blood flow (QICA; Duplex ultrasound) and middle cerebral artery velocity (MCAv; transcranial Doppler ultrasound) were obtained at rest, and during an isooxic hypercapnic (+5 mmHg, +10 mmHg, end-tidal PCO2), and isocapnic hypoxic stress test (50 mmHg and 45 mmHg end-tidal PO2 at sea-level and high-altitude, respectively). All tests were completed before and after unilateral perineural SGB (8-10 mL of 2% lidocaine).
RESULTS:
Heart rate increased at both sea-level and high-altitude post-SGB (sea-level: 7±7 bpm vs. high-altitude: 6±6 bpm, p=0.011). In addition, mean arterial blood pressure increased at both sea-level and high-altitude post-SGB (sea-level: 7±4 mmHg vs. high-altitude: 6±8 mmHg, p=0.005). Resting V̇E was not altered by the SGB (p=0.729) at either sea-level or high-altitude. At sea-level, but not high-altitude, ICA diameter ipsilateral to the blockade trended towards being elevated (p=0.058), while contralateral ICA diameter was elevated (p=0.029) post-SGB. Ipsilateral QICA was elevated post-SGB at sea-level (p=0.036); however, this was not observed in the contralateral QICA. No change in CBF was observed post-SGB at high-altitude data. Blood velocity through the ipsilateral and contralateral MCAs was not influenced by SGB at sea-level and high-altitude (all p≥0.108). At sea-level and high-altitude, the SGB had no impact on ICA and MCA reactivity to hypercapnia (all p≥0.239) and hypoxia (all p≥0.072). At high-altitude, V̇E reactivity to hypercapnia trended towards being elevated (p=0.058), while V̇E reactivity to hypoxia was augmented (p=0.014) post-SGB.
CONCLUSION:
These data indicate that regional removal of SNA via SGB alters resting CBF regulation at sea-level, but not at high-altitude, and it augments chemosensitivity to isooxic hypercapnia and isocapnic hypoxia at high-altitude. Heart rate and mean blood pressure increased to a similar extent at sea-level and high-altitude, without evidence of reflex hyperventilation.