Oxygen-enhanced magnetic resonance (MR)-ventilation imaging of the lung is based on the inhalation of a high concentration of oxygen (hyperoxia). However, the effect of hyperoxia on the pulmonary circulation is not yet fully understood. In this study the impact of hyperoxia on the pulmonary circulation was evaluated.
Ten healthy volunteers were examined in a 1.5 T MRI system with contrast-enhanced perfusion MRI (saturation recovery 2D turboFLASH) of the lung and phase-contrast flow measurements in the pulmonary trunk. Both measurements were performed breathing room air (RA) and, subsequently, 100% oxygen (15 L/min) (O2).
The perfusion measurements showed a significant difference between RA and O2 for the pulmonary blood flow (181 vs. 257 mL/min/100 mL, P = 0.04) and blood volume (14 vs. 21 mL/100 mL, P = 0.008). The mean transit time of the contrast bolus was not changed (P = 0.4) in the dorsal part of the lung, whereas it was significantly prolonged (P = 0.006) in the central part.
The mean heart rate during flow measurements breathing RA (67 ± 11 beats/min) and O2 (61 ± 12 beats/min) were not significantly different (P = 0.055). The average cardiac output (pulmonary trunk) was not significantly lower while breathing O2 (RA: 5.9 vs. O2: 5.5 L/min, P = 0.054).
Hyperoxia causes a significant increase and redistribution of the pulmonary perfusion, whereas it leads to a not significant decrease in cardiac output. Thus, for MR-perfusion and MR-flow measurements oxygen inhalation should be avoided, if possible. In the context of oxygen-enhanced MR-ventilation imaging of the lung the contribution of this effect needs to be further evaluated.
From the *Department of Pediatric Radiology, Children's Hospital University Heidelberg, Heidelberg, Germany; the departments of †Radiology and ‡Medical Physics in Radiology, German Cancer Research Center (DKFZ), Heidelberg, Germany; and §Department of Radiology, Kobe University Graduate School of Medicine, Hyogo, Japan.
Received August 9, 2006, and accepted for publication, after revision, December 23, 2006.
This work was supported by DFG Grant FOR 474-2.
Sebastian Ley and Michael Puderbach contributed equally.
Reprints: Sebastian Ley, MD, Department of Radiology (E010), German Cancer Research Center (DKFZ), Im Neuenheimer Feld 280, 69120 Heidelberg. Germany. E-mail: email@example.com.