2014
DOI: 10.3357/asem.3736.2014
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Individual Susceptibility to High Altitude and Immersion Pulmonary Edema and Pulmonary Lymphatics

Abstract: Subjects susceptible to HAPE/IPE had lower lung density, significantly lower lung mass, and fewer interlobular septa than subjects resistant to HAPE/IPE, suggesting a smaller pulmonary lymphatic network. The observed differences in lymphatics could represent either predisposing factors to, or sequelae of, these potentially lethal conditions.

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Cited by 17 publications
(12 citation statements)
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“…Bronchoalveolar lavage analysis ruled out an inflammatory process as the background for the development of oedema [38]. The prevailing theory claims that several factors, such as increased intrathoracic blood volume and cardiac output, increased pulmonary vasoconstriction and an individually smaller pulmonary lymphatic network contribute to increased hydrostatic pressure that leads to pulmonary capillary stress failure [38,39]. High pulmonary vascular pressure occurs during immersion as a result of a central blood volume shift, augmented by active vasoconstriction in cold water and the diving reflex [40].…”
Section: Noncardiogenic Oedema and Haemoptysismentioning
confidence: 99%
“…Bronchoalveolar lavage analysis ruled out an inflammatory process as the background for the development of oedema [38]. The prevailing theory claims that several factors, such as increased intrathoracic blood volume and cardiac output, increased pulmonary vasoconstriction and an individually smaller pulmonary lymphatic network contribute to increased hydrostatic pressure that leads to pulmonary capillary stress failure [38,39]. High pulmonary vascular pressure occurs during immersion as a result of a central blood volume shift, augmented by active vasoconstriction in cold water and the diving reflex [40].…”
Section: Noncardiogenic Oedema and Haemoptysismentioning
confidence: 99%
“…The risk factors associated with development of HAPE are the rate of ascent ( >350 m per day above 2000 m), the genetic and physiological constitution of the individual, race and family of the individual, the altitude traversed (especially sleeping altitude), any previous history of HAPE, exertion/exercise (particularly high-intensity exercise), cold, administration/intake of any sedatives, any recent infections or disease affecting the lower airways and an idiopathic tendency of pulmonary hypertension [9,[13][14][15][16][17][18][19].…”
Section: Symptoms and Risk Factorsmentioning
confidence: 99%
“…These, susceptible individuals had marked differences in characters like lung volume, lung density, lung mass, number of interlobular septa in lungs, PAP levels and nasal transepithelial potential differences at rest. These evidence indicated towards a genetic and cellular component in the etiology of HAPE [13,21,[24][25][26][27][28]. A number of genomic studies had been performed using global genomics approaches such as microarray or using targeted approaches such as qPCR to determine the association of genes with HAPE susceptibility.…”
Section: Evidences From Genomicsmentioning
confidence: 99%
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“…This fluid shift can aggravate existing chronic conditions that compromise cardiac and pulmonary function. Carter et al 27 used quantitative measures of lung computed-tomographic density to identify anatomic correlates in individuals who were prone to IPE or high-altitude pulmonary edema (HAPE). They measured lung tissue density, total lung mass, and the thickness Figure 2.…”
mentioning
confidence: 99%