View clinical trials related to Acute Mountain Sickness.
Filter by:The trial investigates changes in metabolism during high altitude expedition up to 6865m. A mass-spectrometry based platform is used to detect different oxidative stress related metabolites. Symptoms of acute mountain sickness are evaluated and correlated with laboratory parameters.
Acute mountain sickness is a common ailment in people venturing over 2500 m altitude. Pilgrims to high altitudes are at an added risk since they are unaware and they gain height faster than the recommendations. Acetazolamide is the standard treatment and prophylaxis of acute mountain sickness. There are no randomized controlled trials that have studied protective effects of Acetazolamide in rapid ascent, and there are few conflicting studies regarding this matter. This study is a randomized, double blinded, placebo controlled trial of Acetazolamide versus placebo in 380 healthy individuals travelling to Gosaikunda Lake of Nepal in rates of ascent that are faster than the recommendations. Acetazolamide 125 mg twice daily and a placebo will be randomly assigned for 3 days and participants will be assessed at 3 stations. This study will undertake to establish the role of Acetazolamide in Rapid Ascent and will be the first RCT done in this issue. The investigators hypothesize that Acetazolamide 125mg twice daily given before rapid ascent to high altitude in Nepalese pilgrims will not be superior to placebo in decreasing both the incidence and severity of acute mountain sickness.
Acute mountain sickness (AMS), high altitude pulmonary edema (HAPE), and high altitude cerebral edema (HACE) are complications of rapid ascent to high altitude. Several features suggest that raised intracranial pressure (ICP) may be an important factor in the pathogenesis of AMS. Magnetic resonance imaging of HACE patients has demonstrated that the oedema in HACE is of the vasogenic, rather that cytotoxic, type. Thus it is likely that cerebrovascular permeability has an important role in the development of AMS and HACE. Reactive oxygen species (ROS) have been shown to alter the permeability of the blood-brain barrier in severe ischaemia, causing vasogenic cerebral oedema. Endogenous antioxidant systems may have some capacity to respond to oxidative stress in hypoxia. The plasma concentration of urate, a powerful endogenous antioxidant, rises on acute exposure to high altitude and may play a crucial antioxidant role in systemic hypoxia. This antioxidant prevents free-radical induced cerebral oedema in animal models. There are numerous sources of ROS in hypoxia, including the mitochondrial electron transfer chain, haemoglobin (Hb) autoxidation and xanthine oxidase activity. There have been several reports of raised markers of oxidative stress in humans at moderate altitude (<3000m). Oral antioxidant supplementation with preparations containing vitamins C and E in humans at altitude has been shown to decrease breath pentanes (a marker of oxidative stress), and improve erythrocyte filterability. In a small randomised controlled trial, Bailey and Davies demonstrated a significant reduction in symptoms of AMS in subjects taking an oral antioxidant cocktail. The antioxidants alpha-lipoic acid, vitamin C and vitamin E act synergistically to provide membrane protection from free radical damage, and may protect against hypoxia-induced vascular leakage. We hypothesised that this combination of antioxidants would reduce the severity of acute mountain sickness, and reduce pulmonary artery pressures, in healthy lowlanders acutely exposed to high altitude.
The purpose of this study is to determine whether regular oral use of sildenafil citrate can prevent or attenuate high altitude illnesses.
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.
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.