Cerebral blood flow velocity responses to hypoxia in subjects who are susceptible to high-altitude pulmonary oedema

Abstract

Cerebral blood flow increases on exposure to high altitude, and perhaps more so in subjects who develop acute mountain sickness. We determined cerebral blood flow by transcranial Doppler ultrasound of the middle cerebral artery at sea level, in normoxia (fraction of inspired O2, F(I)O2 0.21), and during 15-min periods of either hypoxic (F(I)O2 0.125) or hyperoxic (F(I)O2 1.0) breathing, in 7 subjects with previous high-altitude pulmonary oedema, 6 climbers who had previously tolerated altitudes between 6000 m and 8150 m, and in 20 unselected controls. Hypoxia increased mean middle cerebral artery flow velocity from 69 (3) to 83 (4) cm x s(-1) (P<0.001) in the controls, from 63 (3) to 75 (3) cm x s(-1) (P<0.001) in the high-altitude pulmonary-oedema-susceptible subjects, and from 58 (4) to 70 (4) cm x s(-1) (P<0.001) in the successful high-altitude climbers. Hyperoxia decreased mean middle cerebral flow velocity to 60 (3) cm x s(-1) (P<0.001), 53 (3) cm x s(-1) (P<0.01), and 49 (3) cm x s(-1) (P<0.01) in the controls, high-altitude pulmonary-oedema-susceptible, and high-altitude climbers, respectively. We conclude that a transcranial Doppler-based estimate of cerebral blood flow is affected by hypoxic and hyperoxic breathing, and that it is not predictive of tolerance to high altitude.

Cerebral hemodynamic characteristics of acute mountain sickness upon acute high-altitude exposure at 3,700 m in young Chinese men

“…Velocities in the MCAs increased immediately upon acute exposure to high altitude, which was the same as the results reported in several studies (Berre et al 1999 ; Lucas et al 2011 ; Rootwelt et al 1986 ; Rudzinski et al 2007 ). We also found that the velocities of BA and VAs, which constitute the posterior cerebral circulation, were significantly altered from 500 to 3,700 m, which is partially consistent with a previous study (Huang et al 1987 ).…”

“…However, the controversy result that CBF increases with acute hypoxia has been reported (Lassen 1992 ). Although a depression chamber study of 10 subjects has showed that AMS is not related to CBF (Baumgartner et al 1999 ), CBF velocity responses to hypoxia in subjects who are susceptible to high-altitude pulmonary edema have been revealed (Berre et al 1999 ).…”

“…Of note, most of these previous studies were conducted with small population sizes and based on simulations or only focused on the velocity of the middle cerebral artery (MCA) (Berre et al 1999 ; Lucas et al 2011 ; Rootwelt et al 1986 ). Furthermore, the velocity of the unilateral MCA was applied as an evaluation or substitute for CBF, and the asymmetry of the bilateral cerebrovascular velocities has not been considered.…”

Prognostic Value of Cerebral near Infrared Spectroscopy and Cerebral Blood Flow Velocity for Developing Acute Mountain Sickness at High Altitudes

“…10 At this time, few studies exist which use cerebral near infrared (NIR) spectroscopy successfully at high altitude [11][12][13][14][15][16][17] and only some investigators have measured the blood fl ow velocity in cerebral arteries. [18][19][20][21][22][23][24] However, the results are different and not clear in detail yet. In a previous study by our research group, we found, for the fi rst time, reproducible data using NIR spectroscopy during a trekking tour in the Nepal Himalayas.…”

Regional cerebral blood flow during acute hypoxia in individuals susceptible to acute mountain sickness

“…Berre (Berre et al 1999) demonstrated a 20-23% increase in middle cerebral artery velocity with hypoxia but found no significant difference between AMS-susceptible and AMS-resistant subjects. Using 15 O-H 2 O PET Buck (Buck et al 1998) reported no change in quantified global cerebral blood flow after acute (20 minute) exposure to 3,000 m, but a 36% increase (+7.2 ml/100g/ min) at 4,500 m (i.e.…”