Changes in cerebral blood flow and vasoreactivity to CO(2) measured by Arterial Spin Labeling after 6 days at 4,350 m.

International audienceChanges in cerebral perfusion and CO(2) cerebrovascular reactivity during and immediately after a sojourn at high altitude remain unclear but may be critical for acclimatization. The aim of the present study was to assess the effects of 6days at 4,350m on cerebral perfusion and cerebrovascular reactivity (CVR) to CO(2) by arterial spin labeling (ASL) magnetic resonance imaging at sea level and to compare it with transcranial Doppler (TCD) results at altitude. Eleven healthy male subjects, non-acclimatized to altitude, stayed for 6days at 4,350m (Observatoire Vallot, massif du Mont-Blanc). Prior to the stay and within 6h after returning to sea level, subjects were investigated using pseudo-continuous ASL at 3T during a block-design inhalation paradigm to measure basal cerebral blood flow (CBF) and CO(2) CVR. End-tidal CO(2) (PetCO(2)), respiratory rate, heart rate and oxygen saturation were recorded during the exam. Subjects were also examined using TCD prior to and on day 5 of the stay at altitude to measure blood velocity in the middle cerebral artery (MCAv) and CO(2) CVR. CO(2) CVR was expressed as percent change in ASL CBF or TCD MCAv per mmHg change in PetCO(2). PetCO(2) was significantly decreased during and after altitude. Significant increases in TCD MCAv compared to before altitude measurements were observed on day 5 at altitude (+20.5±15.5 %). Interestingly, ASL CBF remained increased in the MCA and anterior vascular territories (+22.0±24.1 % and 20.5±20.3 %, respectively) after altitude under normoxic conditions. TCD CVR tended to decrease on day 5 at 4,350m (-12.3±54.5 % in the MCA) while the ASL CVR was significantly decreased after altitude (-29.5±19.8 % in the MCA). No correlation was observed between cerebral hemodynamic changes and symptoms of acute mountain sickness at high altitude. In conclusion, prolonged exposure to high altitude significantly increases blood flow during the altitude stay and within 6h after returning to sea level. Decreased CO(2) CVR after prolonged altitude exposure was also observed using ASL. Changes in cerebral hemodynamics with altitude exposure probably involve other mechanisms than the vasodilatory effect of hypoxia only, since it persists under normoxia several hours following the descent