42 research outputs found
Chemoreceptor responsiveness at sea level does not predict the pulmonary pressure response to high altitude
The hypoxic ventilatory response (HVR) at sea level (SL) is moderately predictive of the
change in pulmonary artery systolic pressure (PASP) to acute normobaric hypoxia. However, because of
progressive changes in the chemoreflex control of breathing and acid-base balance at high altitude (HA),
HVR at SL may not predict PASP at HA. We hypothesized that resting peripheral oxyhemoglobin
saturation (SpO2) at HA would correlate better than HVR at SL to PASP at HA. In 20 participants at SL,
we measured normobaric, isocapnic HVR (L/min·-%SpO2
-1) and resting PASP using echocardiography.
Both resting SpO2 and PASP measures were repeated on day 2 (n=10), days 4-8 (n=12), and 2-3 weeks
(n=8) after arrival at 5050m. These data were also collected at 5050m on life-long HA residents (Sherpa;
n=21). Compared to SL, SpO2 decreased from 98.6 to 80.5% (P<0.001), while PASP increased from
21.7 to 34.0mmHg (P<0.001) after 2-3 weeks at 5050m. Isocapnic HVR at SL was not related to SpO2
or PASP at any time point at 5050m (all P>0.05). Sherpa had lower PASP (P<0.01) than lowlanders on
days 4-8 despite similar SpO2. Upon correction for hematocrit, Sherpa PASP was not different from
lowlanders at SL, but lower than lowlanders at all HA time points. At 5050m, whilst SpO2 was not
related to PASP in lowlanders at any point (all R2=0.50), there was a weak relationship in the
Sherpa (R2=0.16; P=0.07). We conclude that neither HVR at SL nor resting SpO2 at HA correlates with
elevations in PASP at HA