{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,17]],"date-time":"2026-09-17T05:35:34Z","timestamp":1789623334818,"version":"build-2803163510"},"reference-count":102,"publisher":"Wiley","issue":"5","license":[{"start":{"date-parts":[[2021,1,18]],"date-time":"2021-01-18T00:00:00Z","timestamp":1610928000000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"funder":[{"DOI":"10.13039\/501100001804","name":"Canada Research Chairs","doi-asserted-by":"publisher","award":["F11\u201002423"],"award-info":[{"award-number":["F11\u201002423"]}],"id":[{"id":"10.13039\/501100001804","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100000377","name":"Dunhill Medical Trust","doi-asserted-by":"publisher","award":["RTF97\/0117"],"award-info":[{"award-number":["RTF97\/0117"]}],"id":[{"id":"10.13039\/501100000377","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["physoc.onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["The Journal of Physiology"],"published-print":{"date-parts":[[2021,3]]},"abstract":"Key points<\/jats:title>\nWe investigated the influence of arterial () with and without acutely elevated arterial pH and bicarbonate ([HCO3<\/jats:sub>\u2013<\/jats:sup>]) on cerebral blood flow (CBF) regulation in the internal carotid artery and vertebral artery.<\/jats:p><\/jats:list-item>\nWe assessed stepwise iso\u2010oxic alterations in (i.e. cerebrovascular CO2<\/jats:sub> reactivity) prior to and following i.v.<\/jats:sc> sodium bicarbonate infusion (NaHCO3<\/jats:sub>\u2013<\/jats:sup>) to acutely elevate arterial pH and [HCO3<\/jats:sub>\u2013<\/jats:sup>].<\/jats:p><\/jats:list-item>\nTotal CBF was unchanged irrespective of a higher arterial pH at each matched stage of , indicating that CBF is acutely regulated by rather than arterial pH.<\/jats:p><\/jats:list-item>\nThe cerebrovascular responses to changes in arterial H+<\/jats:sup>\/pH were altered in keeping with the altered relationship between and H+<\/jats:sup>\/pH following NaHCO3<\/jats:sub>\u2013<\/jats:sup> infusion (i.e. changes in buffering capacity).<\/jats:p><\/jats:list-item>\nTotal CBF was \u223c7% higher following NaHCO3<\/jats:sub>\u2013<\/jats:sup> infusion during isocapnic breathing providing initial evidence for a direct vasodilatory influence of HCO3<\/jats:sub>\u2013<\/jats:sup> independent of levels.<\/jats:p><\/jats:list-item>\n<\/jats:list><\/jats:p><\/jats:sec>Abstract<\/jats:title>Cerebral blood flow (CBF) regulation is dependent on the integrative relationship between arterial (), pH and cerebrovascular tone; however, pre\u2010clinical studies indicate that intrinsic sensitivity to pH, independent of changes in or intravascular bicarbonate ([HCO3<\/jats:sub>\u2013<\/jats:sup>]), principally influences cerebrovascular tone. Eleven healthy males completed a standardized cerebrovascular CO2<\/jats:sub> reactivity (CVR) test utilizing radial artery catheterization and Duplex ultrasound (CBF); consisting of matched stepwise iso\u2010oxic alterations in (hypocapnia: \u20135, \u201310\u00a0mmHg; hypercapnia: +5, +10 mmHg) prior to and following i.v.<\/jats:sc> sodium bicarbonate (NaHCO3<\/jats:sub>\u2013<\/jats:sup>; 8.4%, 50 mEq\u00a050\u00a0mL\u20131<\/jats:sup>) to elevate pH (7.408\u00a0\u00b1\u00a00.020 vs<\/jats:italic>. 7.461\u00a0\u00b1\u00a00.030; P<\/jats:italic>\u00a0<\u00a00.001) and [HCO3<\/jats:sub>\u2013<\/jats:sup>] (26.1\u00a0\u00b1\u00a01.4 vs<\/jats:italic>. 29.3\u00a0\u00b1\u00a00.9 mEq\u00a0L\u20131<\/jats:sup>; P<\/jats:italic>\u00a0<\u00a00.001). Absolute CBF was not different at each stage of CO2<\/jats:sub> reactivity (P<\/jats:italic>\u00a0=\u00a00.629) following NaHCO3<\/jats:sub>\u2013<\/jats:sup>, irrespective of a higher pH (P<\/jats:italic>\u00a0<\u00a00.001) at each matched stage of (P<\/jats:italic>\u00a0=\u00a00.927). Neither hypocapnic (3.44\u00a0\u00b1\u00a00.92 vs<\/jats:italic>. 3.44\u00a0\u00b1\u00a01.05% per\u00a0mmHg ; P<\/jats:italic>\u00a0=\u00a00.499), nor hypercapnic (7.45\u00a0\u00b1\u00a01.85 vs<\/jats:italic>. 6.37\u00a0\u00b1\u00a02.23% per\u00a0mmHg ; P<\/jats:italic>\u00a0=\u00a00.151) reactivity to were altered pre\u2010 to post\u2010NaHCO3<\/jats:sub>\u2013<\/jats:sup>. When indexed against arterial [H+<\/jats:sup>], the relative hypocapnic CVR was higher (P<\/jats:italic>\u00a0=\u00a00.019) and hypercapnic CVR was lower (P<\/jats:italic>\u00a0=\u00a00.025) following NaHCO3<\/jats:sub>\u2013<\/jats:sup>, respectively. These changes in reactivity to [H+<\/jats:sup>] were, however, explained by alterations in buffering between and arterial H+<\/jats:sup>\/pH consequent to NaHCO3<\/jats:sub>\u2013<\/jats:sup>. Lastly, CBF was higher (688\u00a0\u00b1\u00a0105 vs<\/jats:italic>. 732\u00a0\u00b1\u00a089 mL\u00a0min\u20131<\/jats:sup>, 7%\u00a0\u00b1\u00a012%; P<\/jats:italic>\u00a0=\u00a00.047) following NaHCO3<\/jats:sub>\u2013<\/jats:sup> during isocapnic breathing providing support for a direct influence of HCO3<\/jats:sub>\u2013<\/jats:sup> on cerebrovascular tone independent of . These data indicate that in the setting of acute metabolic alkalosis, CBF is regulated by rather than arterial pH.<\/jats:p><\/jats:sec>","DOI":"10.1113\/jp280682","type":"journal-article","created":{"date-parts":[[2021,1,7]],"date-time":"2021-01-07T16:06:55Z","timestamp":1610035615000},"page":"1439-1457","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":33,"title":["Arterial carbon dioxide and bicarbonate rather than pH regulate cerebral blood flow in the setting of acute experimental metabolic alkalosis"],"prefix":"10.1113","volume":"599","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-6072-7277","authenticated-orcid":false,"given":"Hannah G.","family":"Caldwell","sequence":"first","affiliation":[{"name":"Centre for Heart, Lung and Vascular Health School of Health and Exercise Sciences University of British Columbia Okanagan Kelowna BC Canada"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-1133-2444","authenticated-orcid":false,"given":"Connor A.","family":"Howe","sequence":"additional","affiliation":[{"name":"Centre for Heart, Lung and Vascular Health School of Health and Exercise Sciences University of British Columbia Okanagan Kelowna BC Canada"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-4624-4003","authenticated-orcid":false,"given":"Carter J.","family":"Chalifoux","sequence":"additional","affiliation":[{"name":"Centre for Heart, Lung and Vascular Health School of Health and Exercise Sciences University of British Columbia Okanagan Kelowna BC Canada"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-5657-0059","authenticated-orcid":false,"given":"Ryan L.","family":"Hoiland","sequence":"additional","affiliation":[{"name":"Department of Anesthesiology Pharmacology and Therapeutics Vancouver General Hospital University of British Columbia Vancouver BC Canada"},{"name":"Department of Cellular and Physiological Sciences University of British Columbia Vancouver BC Canada"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-7236-1348","authenticated-orcid":false,"given":"Jay M. 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