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Production of hypoxia-induced corneal edema in aged eyes.
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OBJECTIVE
Corneal thickness assessment is a common clinical procedure applied in corneal and contact lens care. This study aims to investigate the effect of age on hypoxia-induced corneal swelling.
METHODS
Eighteen male subjects were equally divided into the younger [(23.7 +/- 0.8) years old] and
Persistent gastric mucosal hypoxia and interstitial edema after hemorrhagic shock: prevention with steroid therapy.
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To define the role of the nutrient microvasculature in the pathogenesis of acute gastric mucosal erosions, a correlation was performed of changes in intracellular oxygenation (ICPO2) and intracellular potential difference (ICPD) in surface epithelial cells with the histological alterations in the
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
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
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
Effect of hypoxia or hyperbaric oxygen on cerebral edema following moderate fluid percussion or cortical impact injury in rats.
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This study was designed to evaluate the production of cerebral edema [as measured by tissue specific gravity (SpG)] following moderate fluid percussion (FP) and cortical impact (CI) injury in rodents. To determine the effects of a secondary systemic insult, hypoxia (13% oxygen for 30 min) was added
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
Overactivation of corticotropin-releasing factor receptor type 1 and aquaporin-4 by hypoxia induces cerebral edema.
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Cerebral edema is a potentially life-threatening illness, but knowledge of its underlying mechanisms is limited. Here we report that hypobaric hypoxia induces rat cerebral edema and neuronal apoptosis and increases the expression of corticotrophin releasing factor (CRF), CRF receptor type 1 (CRFR1),
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
Pulmonary neuroendocrine cell hyperplasia in hemoglobin Bart-induced hydrops fetalis: A model for chronic intrauterine hypoxia.
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The pulmonary neuroendocrine system includes pulmonary neuroendocrine cells (PNECs) and neuroepithelial bodies (NEBs) that are distributed throughout respiratory epithelium, and regulate lung growth and maturation antenatally. Abnormalities in this system have been linked to many hypoxia-associated
Pulmonary Neuroendocrine Cell Hyperplasia in Hemoglobin Bart-induced Hydrops Fetalis: A model for Chronic Intrauterine Hypoxia.
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The pulmonary neuroendocrine system includes pulmonary neuroendocrine cells (PNECs) and neuroepithelial bodies (NEBs) that are distributed throughout respiratory epithelium and regulate lung growth and maturation antenatally. Abnormalities in this system have been linked to many hypoxia-associated
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
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