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pulmonary edema/hypoxia
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High Altitude Pulmonary Edema in a Mining Worker With an Abnormal Rise in Pulmonary Artery Pressure in Response to Acute Hypoxia Without Prior History of High Altitude Pulmonary Edema.
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High altitude pulmonary edema (HAPE) is a potentially life-threatening form of noncardiogenic pulmonary edema that may develop in otherwise healthy individuals upon ascent to high altitude. A constitutional susceptibility has been noted in some individuals, whereas others appear not to be
Further studies on pulmonary oedema of high altitude. Abnormal responses to hypoxia of men who had developed pulmonary oedema at high altitude.
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101 Indian soldiers, 57 of whom had developed pulmonary oedema of high altitude (POHA) and 44 who had not developed this condition in spite of being at high altitudes for over 2 years, were investigated for observing the differences, if any, in their reaction to acute hypoxic stress. Each subject
Cerebral blood flow velocity responses to hypoxia in subjects who are susceptible to high-altitude pulmonary oedema.
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Cerebral blood flow increases on exposure to high altitude, and perhaps more so in subjects who develop acute mountain sickness. We determined cerebral blood flow by transcranial Doppler ultrasound of the middle cerebral artery at sea level, in normoxia (fraction of inspired O2, F(I)O2 0.21), and
Hypoxemia and low Crs in vagally denervated lambs result from reduced lung volume and not pulmonary edema.
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Vagal denervation performed in the intrathoracic region in newborn lambs leads to hypoxemia and decreased respiratory system compliance (Crs), which could result from atelectasis and/or pulmonary edema. The objective of the present study was to quantify the relative roles of alveolar derecruitment
The Influence of CO2 and Exercise on Hypobaric Hypoxia Induced Pulmonary Edema in Rats.
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Introduction: Individuals with a known susceptibility to high altitude pulmonary edema (HAPE) demonstrate a reduced ventilation response and increased pulmonary vasoconstriction when exposed to hypoxia. It is unknown whether reduced sensitivity to hypercapnia is correlated with increased incidence
Effects of hypobaric hypoxia on vascular endothelial growth factor and the acute phase response in subjects who are susceptible to high-altitude pulmonary oedema.
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In order to investigate whether vascular endothelial growth factor (VEGF) and inflammatory pathways are activated during acute hypobaric hypoxia in subjects who are susceptible to high-altitude pulmonary oedema (HAPE-S), seven HAPE-S and five control subjects were exposed to simulated altitude
G-CSF instillation into rat lungs mediates neutrophil recruitment, pulmonary edema, and hypoxia.
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Activated neutrophils (PMN) have been implicated in the pathogenesis of adult respiratory distress syndrome (ARDS). Granulocyte colony-stimulating factor (G-CSF) is essential for PMN production and activation of PMN functions. We have recently shown that levels of G-CSF mRNA in a rat model of
Heterogeneous pulmonary blood flow in response to hypoxia: a risk factor for high altitude pulmonary edema?
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High altitude pulmonary edema (HAPE) is a rapidly reversible hydrostatic edema that occurs in individuals who travel to high altitude. The difficulties associated with making physiologic measurements in humans who are ill or at high altitude, along with the idiosyncratic nature of the disease and
Holmes-Adie syndrome associated with high altitude pulmonary edema and low chemo-responsiveness to hypoxia.
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A 63-year-old patient with Holmes-Adie syndrome presented an altered peripheral chemoreflex and suffered from high altitude pulmonary edema, suggesting an alteration of sensitive afferent fibers from the peripheral chemoreceptors. Chemo-responsiveness to hypoxia should be explored before any
The Complexity of Diagnosing High-Altitude Pulmonary Edema: A Case Report and Review of the Differential Diagnosis of Greater Than Expected Hypoxemia at Altitude.
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High-altitude pulmonary edema (HAPE) is a common presumptive diagnosis for a patient who experiences significant dyspnea and cyanosis at altitude. In this study, we present a case of a 58-year-old woman who was initially diagnosed with HAPE, although further evaluation revealed the presence of two
Susceptibility to high-altitude pulmonary edema is associated with circulating miRNA levels under hypobaric hypoxia conditions
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Hypobaric hypoxia poses stress to sojourners traveling to high-altitude (HA). A cascade of physiological changes occurs to cope with or adapt to hypobaric hypoxia. However, an insufficient physiological response to the hypoxic condition due to imbalanced vascular homeostasis pathways results in
Genetic adaptation to extreme hypoxia: study of high-altitude pulmonary edema in a three-generation Han Chinese family.
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Organismal response to hypoxia is essential for critical regulation of erythropoiesis, other physiological functions, and survival. There is evidence of individual variation in response to hypoxia as some but not all of the affected individuals develop polycythemia, and or pulmonary and cerebral
Viral respiratory infection increases susceptibility of young rats to hypoxia-induced pulmonary edema.
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Recent clinical observations of a high incidence of preexisting respiratory infections in pediatric cases of high-altitude pulmonary edema prompted us to ask whether such infections would increase the susceptibility to hypoxia-induced pulmonary edema in young rats. We infected weanling rats with
Pulmonary blood flow heterogeneity during hypoxia and high-altitude pulmonary edema.
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Uneven hypoxic pulmonary vasoconstriction has been proposed to expose parts of the pulmonary capillary bed to high pressure and vascular injury in high-altitude pulmonary edema (HAPE). We hypothesized that subjects with a history of HAPE would demonstrate increased heterogeneity of pulmonary blood
Role of posterior hypothalamus in hypobaric hypoxia induced pulmonary edema.
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To investigate the role of posterior hypothalamus and central neurotransmitters in the pulmonary edema due to hypobaric hypoxia, rats were placed in a high altitude simulation chamber (barometric pressure-294.4 mmHg) for 24 h. Exposure to hypobaric hypoxia resulted in increases in mean arterial
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