Augmented hypoxic cerebral vasodilation in man during five days at
3810m altitude.
Jensen, Jrgen B., Bjrn Sperling, John W. Severinghaus, and Niels A.
Lassen.
Department of Clinical Physiology and Nuclear Medicine, Bispebjerg
Hospital, Copenhagen, Denmark, and Department of Anesthesia,
University of California San Francisco CA, 94143
APStracts 2:0505A, 1995.
The fractional increase of cerebral blood flow velocity (fCBFv) from
control with 5 min steps of isocapnic hypoxia and hyperoxic
hypercapnia was measured by transcranial Doppler in 6 sea-level
native men before and during a 5 day sojourn at 3810M altitude to
determine whether cerebral vasoreactivity to low arterial oxygen
saturation (SaO2) gradually increased (as does hypoxic ventilatory
response, HVR) or diminished (adapted, in concert with known slow
fall of CBF) at altitude. Control resting Pco2 was chosen each day
during preliminary hyperoxia to set ventilation to 140 ml/kg/min for
this and the parallel HVR study, attempting to establish control CSF
and brain ECF pH values unaltered by acclimatization. The
relationship of CBF to SaO2 was non-linear, steepening at lower SaO2
. A hyperbolic equation was used to describe hypoxic cerebrovascular
reactivity: where X = fCBFv at 70%. X rose from 0.346+/-0.104 (s.d.)
at sea level to 0.463+/-0.084 on altitude day 5 (p<0.05, by
paired t-test, justified by the a-priori experimental plan). For
comparison with CO2 sensitivity, from these X values we estimate the
rise of CBF in response to a 1% fall of SaO2 at 80% to be 1.30% at
sea level, and 1.74% after 5 days at altitude. CBF sensitivity to
increased PetCO2 (end-tidal) rose from 4.01+/-0.62%/mm Hg at sea
level to 5.12+/-0.79%/mm Hg on day 5 (p<0.05), as expected at
the lower Pco2 due to the logarithmic relationship of Pco2 to CSF pH.
This change was not significant after correcting to log Pco2. We
conclude that the cerebral vascular response to acute isocapnic
hypoxia may increase during acclimatization at high altitude. The
mechanism is unknown but presumably unrelated to the parallel carotid
chemosensitization which, in these subjects, increased hypoxic
ventilatory response (HVR) by 60% in the same 5 day period (from
0.91+/-0.38 to 1.46+/-0.59 s.d. L/min per % fall of SaO2).
Received 15 May 1995; accepted in final form 8 November 1995.
APS Manuscript Number A501-5.
Article publication pending Journal of Applied Physiology.
ISSN 1080-4757 Copyright 1995 The American Physiological Society.
Published in APStracts on 30 November 95