It is well known that hypobaric hypoxia occurs with acute exposure to high altitude, with commonly associated short term symptoms including headache and short of breath. However, the exact underlying physiological cause is still under debate ^[1]. Furthermore, hypobaric hypoxia is also a concomitant with other diseases such as ischemic stroke and epilepsy^[2], hence studying of cerebrovascular response to hypoxia is of great clinical significance. Past attempts include the use of transcranial Doppler (TCD) at high attitude or measure of cerebral blood flow (CBF) in simulated hypoxia, both of which have methodological shortcomings. In this work, 3D ASL at 3.0T was used to monitor the change of CBF to further extend our understanding of hypobaric hypoxia.Ten healthy subjects [5 male; 5 female; 26±3 years old] were recruited for this study after informed consent was obtained. Participants were nonsmokers, physically fit, taking no medication, living at 20-60m and with no previous exposure to high altitude (> 1500m). No alcohol, caffeine, or medication that could affect CBF was consumed during the study period. On day one, subjects flew from Peking to Lhasa (3658m) and spent five days in Lhasa, then returned to Peking. Subjects underwent MRI for 8 times in total. The first, seventh and eighth examinations were conducted in Peking before and after high altitude exposure, while the rest of the examinations were conducted in Lhasa in consecutive days at high altitude. The same 3.0T scanner (GE Discovery MR 750) with an 8-channel head coil (in vivo) was used at the two sites. The MR protocol included anatomical images as well as CBF measurement using 3D ASL. Spatially matching 3D T1 image of was used to extract white matter, gray matter and CSF region (Fig.1), which were then transferred to the CBF map to obtain respective CBF measure for white matter, gray matter and global brain that include both white matter and gray matter.The averaged CBF value of the global brain, white matter and gray matter among the 10 participants at different time points are plotted in Fig.2. Several observations can be made: CBF measurements in GB, WM and GM all had obvious increase and reached their respective peak at the first day at high altitude, and WM showed the largest percentage of increase; after the first day at high altitude, the CBF measurements started to gradually decrease with a small climb on the third day at high altitude; on the fifth day, the CBF returned to that of sea level; it is interesting to note that, the CBF continued to drop after returning to sea level, even below the that at sea level prior to departure.Previous researches on hypobaric hypoxia either resorted to the use TCD or simulated high altitude hypoxia. It has been recently reported that the assumption that the caliber of the artery does not alter at high altitude may not hold^[3]; whereas simulated hypoxia can only achieve short term effects that derivate from reality that long term exposure to hypoxia takes place, either due to high altitude or pathological changes. To our knowledge, this is the first attempt that consistent imaging setup was used for direct CBF measure using 3D ASL is conducted. Our initial findings agree with previous reports that there is an initial increase in CBF at high altitude, and it soon dissipated; also WM showed a larger increase as compared to GM, which could be due to the fact that high altitude edema is primarily located to WM^[4]. On contrary to previous understanding, it was observed that the CBF stayed at a lower level after returning to sea level even after a week, which is hypothesized to be due to Hypocapnic cerebral vasoconstriction and changes of hematocrit. An extension of the temporal axis in this longitudinal study would be needed to further investigate this observation.