Cerebrovascular responses to hypoxia and hypcapnia in high altitude dwellers

Cerebral blood flow is known to increase in response to hypoxia and to decrease with hypocapnia.
It is not known, however, whether these responses are altered in high-altitude dwellers
who are not only chronically hypoxic and hypocapnic, but also polycythaemic. Here we
examined cerebral blood flow responses to hypoxia and hypocapnia, separately and together, in
Andean high-altitude dwellers, including some with chronic mountain sickness (CMS), which
is characterized by excessive polycythaemia. Studies were carried out at high altitude (Cerro de
Pasco (CP), Peru; barometric pressure (PB) 450 mmHg) and repeated, following relief of the
hypoxia, on the day following arrival at sea level (Lima, Peru; PB 755 mmHg). We compared
these results with those from eight sea-level residents studied at sea level. In nine high-altitude
normal subjects (HA) and nine CMS patients, we recorded middle cerebral artery mean blood
flow velocity (MCAVm) using transcranial Doppler ultrasonography, and expressed responses
as changes from baseline.MCAVmresponses to hypoxia were determined by changing end-tidal
partial pressure of oxygen (PET,O2) from 100 to 50 mmHg, with end-tidal partial pressure of
carbon dioxide clamped. MCAVm responses to hypocapnia were studied by voluntary hyperventilation
with PET,O2 clamped at 100 and 50 mmHg. There were no significant differences
between the cerebrovascular responses of the two groups to any of the interventions at either
location. In both groups, the MCAVm responses to hypoxia were significantly greater at Lima
than at CP (HA, 12.1±1.3 and 6.1±1.0%; CMS, 12.5±0.8 and 5.6±1.2%; P <0.01 both
groups). The responses at Lima were similar to those in the sea-level subjects (13.6±2.3%). The
responses to normoxic hypocapnia in the altitude subjects were also similar at both locations
and greater than those in sea-level residents. During hypoxia, both high-altitude groups showed
responses to hypocapnia that were significantly smaller at Lima than at CP (HA, 2.17±0.23 and
3.29±0.34% mmHg−1, P <0.05; CMS, 1.87±0.16 and 3.23±0.24% mmHg−1; P <0.01).
The similarity of the results from the two groups of altitude dwellers suggests that haematocrit
is unlikely to greatly affect cerebrovascular reactivity to hypoxia and hypocapnia. The smaller
vasodilatation to hypoxia and larger vasoconstriction to hypoxic hypocapnia at high altitude
suggest that cerebrovascular responsesmay be impaired at the high altitude, i.e. a maladaptation.
The changes in the responses within less than 24 h at sea level indicate that this impairment is
rapidly reversible.