Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020672 (hypothermia)
 17,327 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Two hundred and fifteen mountaineering accidents occurred in the Sierra Nevada over a 5-year period in climbers on Class V routes. Patients were evaluated for: climbing preparation and training, first aid experience, altitude acclimatization, age, anatomical site of injuries, and cause of the injury. Consideration as to evacuation procedure was also given. The effect of high altitude exposure impairs judgment and muscular coordination and implies poor acclimatization. Acute mountain sickness and hypothermia were documented in 104 patients, the majority of whom sustained injuries resulting from judgmental errors. Ninety-four injuries involved the ankle and lower tibia, an incidence similar to that seen in alpine skiing a decade ago. There were 17 deaths resulting most frequently from head injuries. Few climbers had formal training in basic mountain medicine which was reflected in the poor assessment and management of injuries, with an unnecessary reliance upon others for evacuation. Morbidity and mortality may be lessened by proper climbing preparation--instruction in mountaineering techniques as well as basic mountain medicine--and by prevention of acute mountain sickness and cold injury.
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PMID:Mountaineering accidents in the Sierra Nevada. 686 58

This study measured the pressor and plasma catecholamine response to local hypothermia during adaptation to hypobaric hypoxia. Eight healthy men were studied at rest and after 10 and 45 min of local cooling of one hand and forearm as well as after 30 min of rewarming at sea level and again 24 h and 5 days after rapid, passive transport to high altitude (4,559 m). Acute mountain sickness scores ranged from 5 to 16 (maximal attainable score: 20) on the first day but were reduced to 0-8 by the fifth day. Systolic blood pressure, heart rate, and plasma epinephrine increased on day 1 at altitude compared with sea level but declined again on day 5, whereas diastolic and mean blood pressures continued to rise in parallel with plasma norepinephrine. With local cooling, an increased vasoactive response was seen on the fifth day at altitude. Very high pressures were obtained, and the pressure elevation was prolonged. Heart rate increased twice as much on day 5 compared with the other two occasions. Thoracic fluid index increased with cooling on day 5, suggesting an increase in pulmonary vascular resistance. In conclusion, prolonged hypoxia seems to elicit an augmented pressor response to local cooling in the systemic and most likely also the pulmonary circulation.
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PMID:Blood pressure and plasma catecholamines in acute and prolonged hypoxia: effects of local hypothermia. 1060 Nov 49

Acute mountain sickness (AMS) develops within a few hours after arrival at high altitude and includes headache, anorexia, nausea, vomiting, and malaise. This afflicts 15-25% of the general tourist population at moderate altitudes. High-altitude cerebral edema (HACE) is considered to be the end stage of severe AMS and has been suggested to be a vasogenic edema, raising the possibility that acute hypoxia may increase blood-brain barrier (BBB) permeability. At present, there are no good small-animal models to study this syndrome. We hypothesize 1) that acute hypoxia can damage the BBB and 2) that rat can be used as a model to study hypoxia-induced changes in BBB permeability, especially if hypoxia-induced hypothermia could be minimized with high ambient temperature (HAT). Male Wistar rats were exposed to 1, 2, and 7 days of hypobaric hypoxia (equivalent to 0.5 atm), and changes in the temperature and BBB permeability were studied. The extravasation of endogenous immunoglobulin G, a large molecule, did not increase during room temperature hypoxia but did increase when hypoxia was combined with HAT. Hypoxia caused a significant increase in the leakage of sodium fluorescein (mol wt 376 Da). The expression of endothelial barrier antigen (EBA), a protein associated with the BBB, was reduced to 50% between 24 and 48 h after exposure to hypoxia, and the loss was exacerbated by HAT. The values almost returned to control levels by 7 days, showing adaptation to hypoxia. Hypoxic rats exhibited sodium fluorescein leakage mainly in focal areas in the brain parenchyma. In conclusion, it is possible to have transient BBB damage through exposure to acute hypoxia, and this damage is exacerbated by increasing body temperature to more of a normothermic value.
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PMID:Effects of acute hypoxia and hyperthermia on the permeability of the blood-brain barrier in adult rats. 1964 26