saturation (SaO2), oxygen uptake (VO2), ventilation (VE), PaO2, PCO2, pH, p50 and lactate
(arterialized capillary blood) were measured. Results: Both groups showed a progressive
reduction in PO and VO2max in hypoxia but decrement was larger in TS than in US at and above
3500m. TS had a greater reduction in HRmax and SaO2. VEmax was greater in TS but not
modified by hypoxia. There was no difference in exercise pH, p50 and lactate between the 2
groups. Conclusion: The decline in aerobic performance (VO2max and PO) in acute hypoxia is
larger in TS at and above 3500m. This decrement is correlated with HRmax decline and with
SaO2 level at maximal exercise. A greater reduction in maximal O2 transport in TS could explain
the differences between the 2 populations. To explain the higher desaturation in TS, several
explanations can be put forward 1) decrease in O2 transport limited to a lower HRmax. 2) A
lower O2 mixed venous saturation (SvO2) in TS associated with an alveolar-capillary diffusion
limitation. We hypothesize that US could drop SvO2 until 4500m but TS only until 2500m. Thus
at and above 3500m, the largest arterial-venous O2 difference decrement in TS could explain
their greater decrement in aerobic performance.
158.
WEATHER AND DEATH ON MOUNT EVEREST: AN ANALYSIS OF HIGH IMPACT
STORMS AT EXTREME ALTITUDE. Kent Moore
1
, John Semple
1
. University of Toronto
1
.
Scientific interest in Mount Everest has been largely focused on the hypoxia caused by the
summit's low barometric pressure. Although weather is recognized as a significant risk for
climbers on the mountain, it has not been extensively studied. Through the use of recent
observations made at an elevation of 7,986m on the mountain's South Col and other datasets, we
show that high impact weather events on Mount Everest, including the May 1996 storm in which
8 climbers perished, are often associated with large-scale intrusions of stratospheric air into the
upper-troposphere. We will show that the magnitude of the drop in barometric pressure, PO2 and
VO2max associated with these events is as large as that estimated to occur between summer and
winter on Mount Everest. We therefore argue that these changes are of physiological significance
and these high impact weather events may play a role in the fatalities that occur on Mount
Everest. This is especially true above 7000m, where climbers are at the limits of endurance and
drops in barometric pressure of the magnitude that we have established, when compounded by the
accumulative effect of hypoxia, fatigue, high winds, extreme cold and incomplete
acclimatization, could shift a coping climber from a state of brittle tolerance to physiological
distress.
159.
THERAPEUTIC EFFECTS OF L-ARGININE ON HIGH ALTITUDE PULMONARY EDEMA.
Xinbing Mou
1
, Yuqi Gao
2
, Fuyu Liu
2
, Ganglin Ye
1
, Hongya Tang
1
. High Altitude Medical
Research Center, The Military General Hospital of Tibet, Tibet, China;
1
, Department of
Pathophysiology and High Altitude Physiology, Third Military Medical University, Chong
2
.
High altitude pulmonary edema ( HAPE ) is a life threatening condition. The pathogenesis
and treatment of HAPE remain obscure. This study was designed to evaluate the clinical curative
effects of L-arginine in patients with HAPE. Eight patients with HAPE undergone Swan-Ganz
catheter. The parameters of hemodynamics and arterial blood gases in HAPE were measured
before and after administration of L-arginine. The clinical severity of HAPE was assessed by
using the Lake Louise acute mountain sickness scoring system. After injecting intravenously L-
arginine, the mPAP, PVR of HAPE decreased significantly as compared with that piror to
injection; the Lake Louise scores of HAPE also decreased significantly as compared with the
values piror to injection; the PaO2 and SaO2 of HAPE were increased; the systemic blood
pressure, heart rate were not different before and after injecting L-arginine. Results suggested L-
arginine may improve the clinical symptoms of the patients with HAPE; It also can selectively
decline the pulmonary hypertension in HAPE without causing systemic vasodilation.(By grant of
01L062).
