View clinical trials related to Altitude Sickness.
Filter by:The trial evaluates the role of ascent protocol on acute mountain sickness and cardio-respiratory physiology during an ascent to Muztagh Ata (7546m). Two groups of mountaineers ascend with different acclimatization time to the summit. The prevalence and severity of symptoms of acute mountain sickness are evaluated along with physiologic variables.
Acclimatization by mountaineering prior to high altitude sojourns have shown to be effective in prevention of acute mountain sickness (AMS). The aim of this study is to investigate whether intermittent exposure to normobaric hypoxia during sleep is also effective to prevent AMS.
It has been shown, that subjects susceptible to high altitude pulmonary edema (HAPE)are characterized by an abnormal increase of pulmonary artery pressure at rest in hypoxia and during exercise in normoxia. This abnormal rise of pulmonary artery pressure has also been observed in about 10 % of otherwise healthy subjects without prior altitude exposure. The aim of the study is to investigate the susceptibility to HAPE in unacclimatized subjects with abnormal increase of pulmonary artery pressure at rest in hypoxia and during exercise in normoxia after rapid ascent to high altitude (4559 m).
The prevalence of High Altitude Polycythemia (or Chronic Mountain Sickness) is between 8 and 15% in the high altitude regions of South America. There is no pharmacological treatment available. After a first preliminary study in 2003 demonstrating the beneficial effects of acetazolamide in reducing hematocrit in these patients, after 3 weeks of treatment, we want to confirm this effect and implement a treatment protocol of 3 month-duration.
Commercial aircraft passengers are exposed to atmospheric pressures ranging from the pressure found at ground level to that encountered in the external environment at 8,000 feet. There is some evidence in the medical literature that symptoms of acute mountain sickness can result from ascent to altitudes of 6,300 to 10,000 feet by unacclimated persons during the first few days following ascent, probably due to the hypoxia that results from breathing air at the reduced ambient pressures at altitude. The logical hypothesis that follows is that exposure to 8,000 feet could cause hypoxia sufficient to adversely affect the comfort and well being of some commercial aircraft passengers on prolonged flights. There is insufficient data in the literature to validate this hypothesis. Exercise at sea level and at altitude reduces arterial oxygen levels. The logical hypothesis that follows is that the combination of moderate exercise and exposure to altitude could cause hypoxia sufficiently severe to adversely affect the comfort and well being of some people and that the combined effect of exercise and altitude on comfort and well being is greater than the effect of exercise or altitude alone. Again, there is insufficient evidence in the literature to substantiate this possibility. The purpose of this investigation is to test these hypotheses.
A double-blind placebo controlled study - To compare the effect of tadalafil and dexamethasone versus placebo on Ppa and pulmonary edema formation in subjects susceptible to HAPE. - To investigate the effect of dexamethasone on alveolar fluid clearance, as assessed by measurement of the nasal potential difference, and prevention of HAPE. - To investigate the effect of the tadalafil and dexamethasone versus placebo on the dynamic CBF autoregulation properties and on the development of AMS in HAPE susceptible subjects.
This study is is the first step of a full study named CHEMOGENE because it explores the genetic determinant of an alteration of the chemoreflex. This reflex determines hyperventilation when the pressure of oxygen falls in the blood. This happens when subjects travel to high-altitude where oxygen levels diminish in the atmosphere. Subjects with such an altered chemoreflex are intolerant to altitude and develop pulmonary or cerebral edema associated with a severe headache. In this study we compare subjects tolerant to high altitude (8000 meters)to subjects intolerant to altitude. The chemoreflex is measured i.e. the hyperventilation associated with hypoxia and all subjects are scanned for the genes implicated in the mitochondrial respiratory chain. The idea is that subjects with an impaired oxygen sensing will exhibit an altered chemoreflex and will be intolerant to high-altitude.