{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,2,26]],"date-time":"2026-02-26T21:34:46Z","timestamp":1772141686727,"version":"3.50.1"},"reference-count":46,"publisher":"Wiley","issue":"19","license":[{"start":{"date-parts":[[2020,7,29]],"date-time":"2020-07-29T00:00:00Z","timestamp":1595980800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":["physoc.onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["The Journal of Physiology"],"published-print":{"date-parts":[[2020,10]]},"abstract":"<jats:sec><jats:title>Key points<\/jats:title><jats:p><jats:list list-type=\"bullet\">\n<jats:list-item><jats:p>Changes in haematocrit influence nitric oxide signalling through alterations in shear stress stimuli and haemoglobin scavenging of nitric oxide; these two regulatory factors have not been assessed simultaneously<\/jats:p><\/jats:list-item>\n<jats:list-item><jats:p>Isovolumic haemodilution led to a marked increase in brachial artery flow\u2010mediated dilatation in humans<\/jats:p><\/jats:list-item>\n<jats:list-item><jats:p>The increase in flow\u2010mediated dilatation occurred in the face of an unaltered shear stress stimulus for vasodilatation and reduced resting steady\u2010state nitric oxide levels in the blood<\/jats:p><\/jats:list-item>\n<jats:list-item><jats:p>Collectively, our data point towards haemoglobin scavenging of nitric oxide as a key regulatory factor of brachial flow\u2010mediated dilatation and highlight the importance of the simultaneous consideration of nitric oxide production and inactivation when investigating vascular function in humans<\/jats:p><\/jats:list-item>\n<\/jats:list><\/jats:p><\/jats:sec><jats:sec><jats:title>Abstract<\/jats:title><jats:p>Haemoglobin (Hb) may impact the transduction of endothelium\u2010dependent and nitric oxide (NO)\u2010mediated vasodilator activity, given its contribution to shear stress stimuli and diverse biochemical reactions with NO. We hypothesized that an acute reduction in [Hb] and haematocrit (Hct) would increase brachial artery flow\u2010mediated dilatation (FMD). In 11 healthy males (28\u00a0\u00b1\u00a07\u00a0years; 23\u00a0\u00b1\u00a02\u00a0kg\u00a0m<jats:sup>\u22122<\/jats:sup>), FMD (Duplex ultrasound), arterial blood gases, Hct and [Hb], blood viscosity, and NO metabolites (ozone\u2010based chemiluminescence) were measured before and after isovolumic haemodilution, where \u223c20% of whole blood was removed and replaced with 5% human serum albumin. Haemodilution reduced Hct by 18\u00a0\u00b1\u00a02% (<jats:italic>P<\/jats:italic>\u00a0&lt;\u00a00.001) and whole blood viscosity by 22\u00a0\u00b1\u00a05% (<jats:italic>P<\/jats:italic>\u00a0&lt;\u00a00.001). Plasma nitrite (<jats:italic>P<\/jats:italic>\u00a0=\u00a00.01), <jats:italic>S<\/jats:italic>\u2010nitrosothiols (<jats:italic>P<\/jats:italic>\u00a0=\u00a00.03) and total red blood cell NO (<jats:italic>P<\/jats:italic>\u00a0=\u00a00.001) were collectively reduced by \u223c15\u201340%. Brachial artery FMD increased by \u223c160% from 3.8\u00a0\u00b1\u00a02.1 to 9.7\u00a0\u00b1\u00a04.5% (<jats:italic>P<\/jats:italic>\u00a0=\u00a00.004). Statistical covariation for the shear stress stimulus did not alter FMD, indicating that the increase in FMD was not directly related to alterations in whole blood viscosity and the shear stimulus. Collectively, these findings indicate that haemoglobin scavenging of NO appears to be an important factor in the regulation of FMD under normal conditions through constraint of endothelium\u2010dependent NO\u2010mediated vasodilatation in healthy humans.<\/jats:p><\/jats:sec>","DOI":"10.1113\/jp280141","type":"journal-article","created":{"date-parts":[[2020,7,8]],"date-time":"2020-07-08T14:24:15Z","timestamp":1594218255000},"page":"4225-4236","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":17,"title":["Acute reductions in haematocrit increase flow\u2010mediated dilatation independent of resting nitric oxide bioavailability in humans"],"prefix":"10.1113","volume":"598","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-5657-0059","authenticated-orcid":false,"given":"Ryan L.","family":"Hoiland","sequence":"first","affiliation":[{"name":"Department of Anaesthesiology, Pharmacology and Therapeutics University of British Columbia  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&amp; Recreation University of Alberta  Edmonton AB Canada"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-2634-6195","authenticated-orcid":false,"given":"Alexander","family":"Patrician","sequence":"additional","affiliation":[{"name":"Centre for Heart, Lung, &amp; Vascular Health, School of Health and Exercise Sciences University of British Columbia\u00a0\u2013\u00a0Okanagan  Kelowna BC Canada"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-0818-6420","authenticated-orcid":false,"given":"Mike","family":"Stembridge","sequence":"additional","affiliation":[{"name":"Cardiff School of Sport and Health Sciences Cardiff Metropolitan University  Cardiff UK"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-1133-2444","authenticated-orcid":false,"given":"Connor A.","family":"Howe","sequence":"additional","affiliation":[{"name":"Centre for Heart, Lung, 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