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UBC Theses and Dissertations

Regulation of cerebral blood flow during transient hypertension in humans Wildfong, Kevin Wayne


Although the role of sympathetic nervous activity (SNA) in cerebral blood flow (CBF) regulation is poorly understood in humans, animal studies have demonstrated that elevations in cerebral SNA may protect against cerebral hyper-perfusion during elevations in blood pressure (BP). We examined the hypothesis that alpha-1 receptor blockade (Prazosin) would augment increases in CBF during acute hypertension. In 15 healthy volunteers, beat-by-beat BP, extra-cranial artery blood flow (internal carotid artery (QICA) & vertebral artery (QVA)), intra-cranial artery velocity (middle cerebral artery (MCAv) & posterior cerebral artery (PCAv)), and end-tidal gases (PETO₂ & PETCO₂) were controlled before and 90 min following oral Prazosin (1mg/20kg) at rest and during transient hypertension. Hypertension was non-pharmacologically induced using 30% maximal voluntary contraction (MVC) handgrip exercise (HG), lower-body positive pressure (LBPP), and combined LBPP & HG (LBPP+HG). Following Prazosin administration, baseline PETCO₂ (-1 mmHg), MAP (-7 mmHg) & MCAv (-5 cm/sec) were all significantly reduced (P<0.05), while PCAv, QICA and QVA and respective diameter were all unchanged; VA velocity was reduced (P=0.03), while ICA velocity was unchanged (P=0.96). Following Prazosin, MAP during 30% MVC HG was unchanged while MAP was significantly reduced during LBPP (-29 ± 68%) and LBPP+HG (-40 ± 38%); despite these changes in MAP, MCAv, PCAv, QICA & QVA all remained unchanged (P>0.05). There was significant attenuation of absolute PCAv CVC following Prazosin during LBPP and LBPP+HG (Δ0.036 ± 0.032 vs. Δ0.007 ± 0.019 & Δ0.053 ± 0.04 vs. Δ0.024 ± 0.025 cm/sec/mmHg; P<0.05), but not HG (P=0.4). Although changes in QICA and MAP were unrelated (r²=0.07; P=0.16) during 30% MVC HG, LBPP & LBPP+HG, QVA was positively correlated (r²=0.14; P=0.02) with changes in MAP following Prazosin. This latter observation is consistent with changes in PCAv CVC, potentially indicative of vasodilation in the PCA or alternatively redistribution of QVA before communicating with the PCA, or both. While these findings are contrary to our hypothesis, these differential findings are interpreted to indicate that there is a disparity between the extra- and intra-cranial arteries and that SNA serves a functional role in the regulation of the posterior region of the brain during transient hypertension.

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