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 (pO(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 pO(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 +/- 7.2years) were scanned using pseudo-continuous ASL in combination with room air (RA; 21% O-2/79% N-2), hypercapnic normoxic (HN; 5% CO2/21% O-2/74% N-2) and hypercapnic hyperoxic (HH; 5% CO2/95% 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 +/- 13.3years) 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 1.65s at baseline to 1.49 +/- 0.07s 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 +/- 8.2mL/100g/min; HH CBF=45.2 +/- 13.9mL/100g/min). It can be concluded that hyperoxic (95% O-2) 3-T arterial blood T-1aHH=1.49 +/- 0.07s relative to a normoxic T-1a of 1.65s. Copyright (c) 2015 John Wiley & Sons, Ltd.