In vivo quantification of hyperoxic arterial blood water T 1

Normocapnic hyperoxic and hypercapnic hyperoxic gas challenges are increasingly being used in cerebrovascular reactivity (CVR) and calibrated functional MRI experiments. The longitudinal arterial blood water relaxation time ( T 1a ) change with hyperoxia will influence signal quantification through mechanisms relating to elevated partial pressure of plasma‐dissolved O 2 ( p O 2 ) and increased oxygen bound to hemoglobin in arteries ( Y a ) and veins ( Y v ). The dependence of T 1a on Y a and Y v has been elegantly characterized ex vivo ; however, the combined influence of p O 2 , Y a and Y v on T 1a in vivo under normal ventilation has not been reported. Here, T 1a is calculated during hyperoxia in vivo by a heuristic approach that evaluates T 1 ‐dependent arterial spin labeling (ASL) signal changes to varying gas stimuli. Healthy volunteers ( n  = 14; age, 31.5 ± 7.2 years) were scanned using pseudo‐continuous ASL in combination with room air (RA; 21% O 2 /79% N 2 ), hypercapnic normoxic (HN; 5% CO 2 /21% O 2 /74% N 2 ) and hypercapnic hyperoxic (HH; 5% CO 2 /95% O 2 ) gas administration. HH T 1a was calculated by requiring that the HN and HH cerebral blood flow (CBF) change be identical. The HH protocol was then repeated in patients ( n  = 10; age, 61.4 ± 13.3 years) with intracranial stenosis to assess whether an HH T 1a decrease prohibited ASL from being performed in subjects with known delayed blood arrival times. Arterial blood T 1a decreased from 1.65 s at baseline to 1.49 ± 0.07 s 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 = 36.6 ± 8.2 mL/100 g/min; HH CBF = 45.2 ± 13.9 mL/100 g/min). It can be concluded that hyperoxic (95% O 2 ) 3‐T arterial blood T 1aHH  = 1.49 ± 0.07 s relative to a normoxic T 1a of 1.65 s. Copyright © 2015 John Wiley & Sons, Ltd.