Augmented hypoxic cerebral vasodilation in men during 5 days at 3,810 m altitude
J. B. Jensen, B. Sperling, J. W. Severinghaus and N. A. Lassen Department of Clinical Physiology and Nuclear Medicine, Bispebjerg Hospital, Copenhagen, Denmark. The fractional increase in cerebral blood flow (CBF) velocity (VCBF) from the control value with 5-min steps of isocapnic hypoxia and hyper...
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Veröffentlicht in: | Journal of applied physiology (1985) 1996-04, Vol.80 (4), p.1214-1218 |
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Zusammenfassung: | J. B. Jensen, B. Sperling, J. W. Severinghaus and N. A. Lassen
Department of Clinical Physiology and Nuclear Medicine, Bispebjerg Hospital, Copenhagen, Denmark.
The fractional increase in cerebral blood flow (CBF) velocity (VCBF) from
the control value with 5-min steps of isocapnic hypoxia and hyperoxic
hypercapnia was measured by transcranial Doppler in six sea-level native
men before and during a 5-day sojourn at 3,810 m altitude to determine
whether cerebral vasoreactivity to low arterial O2 saturation (SaO2)
gradually increased [as does the hypoxic ventilatory response (HVR)] or
diminished (adapted, in concert with known slow fall of CBF) at altitude. A
control resting PCO2 value was chosen each day during preliminary hyperoxia
to set ventilation at 140 ml.kg-1.min-1 for this and the parallel HVR
study, attempting to establish control cerebrospinal fluid (CSF) and brain
extracellular fluid pH values unaltered by acclimatization. The
relationship of CBF to SaO2 was nonlinear, steepening at a lower SaO2. A
hyperbolic equation was used to describe hypoxic cerebrovascular
reactivity: fractional VCBF = x[60/ (SaO2-40)-1], where X is the fractional
increase of VCBF at 70%.X rose from 0.346 +/- 0.104 (SD) 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 in CBF in response to a 1% fall
in SaO2 at 80% to be 1.30% at sea level and 1.74% after 5 days at altitude.
CBF sensitivity to increased end-tidal PCO2 rose from 4.01 +/- 0.62%/Torr
at sea level to 5.12 +/- 0.79%/Torr 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 correction 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 is
presumably unrelated to the parallel carotid chemosensitization that, in
these subjects, increased the HVR by 60% in the same 5-day period from 0.91
+/- 0.38 to 1.46 +/- 0.59 l.min-1.% fall in SaO2-1). |
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ISSN: | 8750-7587 1522-1601 |
DOI: | 10.1152/jappl.1996.80.4.1214 |