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The longitudinal arterial blood water relaxation time (<jats:italic>T<\/jats:italic><jats:sub>1a<\/jats:sub>) change with hyperoxia will influence signal quantification through mechanisms relating to elevated partial pressure of plasma\u2010dissolved O<jats:sub>2<\/jats:sub> (<jats:italic>p<\/jats:italic>O<jats:sub>2<\/jats:sub>) and increased oxygen bound to hemoglobin in arteries (<jats:italic>Y<\/jats:italic><jats:sub>a<\/jats:sub>) and veins (<jats:italic>Y<\/jats:italic><jats:sub>v<\/jats:sub>). The dependence of <jats:italic>T<\/jats:italic><jats:sub>1a<\/jats:sub> on <jats:italic>Y<\/jats:italic><jats:sub>a<\/jats:sub> and <jats:italic>Y<\/jats:italic><jats:sub>v<\/jats:sub> has been elegantly characterized <jats:italic>ex vivo<\/jats:italic>; however, the combined influence of <jats:italic>p<\/jats:italic>O<jats:sub>2<\/jats:sub>, <jats:italic>Y<\/jats:italic><jats:sub>a<\/jats:sub> and <jats:italic>Y<\/jats:italic><jats:sub>v<\/jats:sub> on <jats:italic>T<\/jats:italic><jats:sub>1a<\/jats:sub> <jats:italic>in vivo<\/jats:italic> under normal ventilation has not been reported. Here, <jats:italic>T<\/jats:italic><jats:sub>1a<\/jats:sub> is calculated during hyperoxia <jats:italic>in vivo<\/jats:italic> by a heuristic approach that evaluates <jats:italic>T<\/jats:italic><jats:sub>1<\/jats:sub>\u2010dependent arterial spin labeling (ASL) signal changes to varying gas stimuli. Healthy volunteers (<jats:italic>n<\/jats:italic>\u2009=\u200914; age, 31.5\u2009\u00b1\u20097.2\u2009years) were scanned using pseudo\u2010continuous ASL in combination with room air (RA; 21% O<jats:sub>2<\/jats:sub>\/79% N<jats:sub>2<\/jats:sub>), hypercapnic normoxic (HN; 5% CO<jats:sub>2<\/jats:sub>\/21% O<jats:sub>2<\/jats:sub>\/74% N<jats:sub>2<\/jats:sub>) and hypercapnic hyperoxic (HH; 5% CO<jats:sub>2<\/jats:sub>\/95% O<jats:sub>2<\/jats:sub>) gas administration. HH <jats:italic>T<\/jats:italic><jats:sub>1a<\/jats:sub> was calculated by requiring that the HN and HH cerebral blood flow (CBF) change be identical. The HH protocol was then repeated in patients (<jats:italic>n<\/jats:italic>\u2009=\u200910; age, 61.4\u2009\u00b1\u200913.3\u2009years) with intracranial stenosis to assess whether an HH <jats:italic>T<\/jats:italic><jats:sub>1a<\/jats:sub> decrease prohibited ASL from being performed in subjects with known delayed blood arrival times. Arterial blood <jats:italic>T<\/jats:italic><jats:sub>1a<\/jats:sub> decreased from 1.65\u2009s at baseline to 1.49\u2009\u00b1\u20090.07\u2009s during HH. In patients, CBF values in the affected flow territory for the HH condition were increased relative to baseline CBF values and were within the physiological range (RA CBF\u2009=\u200936.6\u2009\u00b1\u20098.2\u2009mL\/100\u2009g\/min; HH CBF\u2009=\u200945.2\u2009\u00b1\u200913.9\u2009mL\/100\u2009g\/min). It can be concluded that hyperoxic (95% O<jats:sub>2<\/jats:sub>) 3\u2010T arterial blood <jats:italic>T<\/jats:italic><jats:sub>1aHH<\/jats:sub>\u2009=\u20091.49\u2009\u00b1\u20090.07\u2009s relative to a normoxic <jats:italic>T<\/jats:italic><jats:sub>1a<\/jats:sub> of 1.65\u2009s. Copyright \u00a9 2015 John Wiley &amp; Sons, Ltd.<\/jats:p>","DOI":"10.1002\/nbm.3411","type":"journal-article","created":{"date-parts":[[2015,9,30]],"date-time":"2015-09-30T04:31:43Z","timestamp":1443587503000},"page":"1518-1525","source":"Crossref","is-referenced-by-count":14,"title":["<i>In vivo<\/i> quantification of hyperoxic arterial blood water <i>T<\/i><sub>1<\/sub>"],"prefix":"10.1002","volume":"28","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-5079-2868","authenticated-orcid":false,"given":"Jeroen C. 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