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altitude sickness/калиум
Врската е зачувана во таблата со исечоци
Страница 1 од 30 резултати
Chronic altitude sickness with potassium intoxication; a case report.
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Effects of mitochondrial K(ATP) modulators on cardioprotection induced by chronic high altitude hypoxia in rats.
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OBJECTIVE
Adaptation of rats to intermittent high altitude hypoxia increases the tolerance of their hearts to acute ischemia/reperfusion injury. Our aim was to examine the role of mitochondrial ATP-sensitive potassium channels (K(ATP)) in this form of protection.
METHODS
Adult male Wistar rats were
Can migraine prophylaxis prevent acute mountain sickness at high altitude?
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Acute mountain sickness (AMS) develops in people trekking at high altitude. The underlying mechanism is vasodilation due to low pressure of oxygen. However, individual susceptibility for AMS is unknown, thus, one cannot predict when or to whom it happens. Because AMS usually begins with headache,
Study of acute mountain sickness during "rapid ascent" trekking to extreme altitude.
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Acute mountain sickness (AMS) is an important cause of morbidity and mortality following acute exposure to high altitude. Several clinical variables were evaluated during the 1990 Trans-Kalindi Exploration to extreme altitude (5949 m) in 10 healthy adult lowlanders (age 31.7 +/- 6.4 yrs) who
Atrial natriuretic peptide, altitude and acute mountain sickness.
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1. To investigate the mechanisms of acute mountain sickness, 22 subjects travelled to 3100 m by road and the following day walked to 4300 m on Mount Kenya. Control measurements were made over 2 days at 1300 m before ascent and for 2 days after arrival at 4300 m. These included body weight, 24 h
Diabetic ketoacidosis and acute mountain sickness: case report and review of treatment options in type 1 diabetes mellitus.
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A 30-year-old man with a 20-year history of well-controlled type 1 diabetes mellitus and no microvascular complications traveled from near sea level to an altitude of 3000 m within 6 hours. At altitude, his blood glucose levels began to rise, necessitating increased insulin delivery. Typical
Birmingham Medical Research Expeditionary Society 1977 Expedition: effect of a Himalayan trek on whole body composition, nitrogen and potassium.
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The body composition of the 17 members of the BMRES was studied using body weight and fat fold calipers, with measurements of whole body potassium and nitrogen. The full assessment was made just before departure from Birmingham and immediately on return. Daily observations of body weight and fat
Adaptation to high altitude hypoxia protects the rat heart against ischemia-induced arrhythmias. Involvement of mitochondrial K(ATP) channel.
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The aim was to determine whether adaptation to chronic hypoxia protects the heart against ischemic arrhythmias and whether ATP-dependent potassium channels (K(ATP)) play a role in the antiarrhythmic mechanism. Adult male rats were adapted to intermittent high altitude hypoxia (5000 m, 4 h/day) and
Effects of aging on the cardiac remodeling induced by chronic high-altitude hypoxia in rat.
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Effects of chronic high-altitude hypoxia on the remodeling of right ventricle were examined in three age groups of rats: 2, 6, and 18 mo. The extent of right ventricular (RV) hypertrophy (RVH) showed an age-associated diminution. RV cell size and pericellular fibrosis showed a significant increase
Enhanced exercise-induced rise of aldosterone and vasopressin preceding mountain sickness.
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A possible contribution of exercise to the fluid retention associated with acute mountain sickness (AMS) was investigated in 17 mountaineers who underwent an exercise test for 30 min on a bicycle ergometer with a constant work load of 148 +/- 9 (SE) W at low altitude (LA) and with 103 +/- 6 W 4-7 h
Evolutionary Adaptation of Aquaporin-4 in Yak (Bos grunniens) Brain to High-Altitude Hypoxia of Qinghai-Tibetan Plateau.
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Ding, Yanping, Jianfeng Liu, Yuanqing Xu, Xiaoqing Dong, and Baoping Shao. Evolutionary adaptation of aquaporin-4 in yak (Bos grunniens) brain to high-altitude hypoxia of Qinghai-Tibetan Plateau. High Alt Med Biol 00:000-000, 2020. Background: In high-altitude animals, brain
Intermittent high altitude hypoxia protects the heart against lethal Ca2+ overload injury.
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Adaptation to intermittent high altitude (IHA) hypoxia can protect the heart against ischemia-reperfusion injury. In view of the fact that both Ca2+ paradox and ischemia-reperfusion injury are associated with the intracellular Ca2+ overload, we tested the hypothesis that IHA hypoxia may protect
Oxygen sensors in the organism: examples of regulation under altitude hypoxia in mammals.
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Oxygen sensing is a determinant function of mammals, especially humans, to maintain their activity under acute or chronic exposure to hypoxia. True O2 sensors (chemoreceptors, erythropoietin secreting cells) are involved in regulation loops, which aim to restore O2 availability to the cells. Pseudo
Ca(2+) sensitivity of fetal coronary arteries exposed to long-term, high-altitude hypoxia.
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OBJECTIVE
To determine the contribution of decreased calcium responsiveness of fetal coronary arteries to decreased contractile responses to potassium and the thromboxane A(2) analogue U46619 in these arteries after exposure to chronic hypoxemia.
METHODS
Concentration-response curves to Ca(2+) in
[Certain changes in the water-electrolyte metabolism in desoxycorticosterone acetate salt hypertension in rats adapted to high altitude hypoxia].
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In the course of the development of desoxycorticosterone-acetate-salt hypertension the animals were noted to display high appetite of sodium chloride, a considerable increase of the weight of the heart, kidneys and adrenal glands, of the diameter of the glomeruli and the surface of the cortical and
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