The effects of acute altitude exposure in swiss highlanders and lowlanders

Koller, E. A.; Leśniewska, B.; Bührer, A.; Bub, Achim; Kohl, J.

doi:10.1007/bf01427056

Cited by 16 publications

(9 citation statements)

References 26 publications

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“…Urinary urodilatin excretion is increased sixfold in the hypoxic isolated perfused kidney [ 116 ]. However, with 1 h of hypoxia in humans there is no increase in urinary urodilantin excretion [ 8 ], or after 24 h at 4,559 m [ 12 ], although in a hypobaric simulation of 6,000 m there was a slight increase [ 117 ]. On the other hand, after 2 days at 4,559 m urinary urodilatin excretion was halved [ 12 ].…”

Section: Natriuretic Peptidesmentioning

confidence: 77%

Renal Function and Fluid Homeostasis

Swenson

Olsen

2013

High Altitude

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Hypoxia can directly affect the kidneys, but more importantly, its effects on systemic acid-base balance, ventilation, neuroendocrine refl exes, and hemodynamics all play a far greater part in altering renal function and fl uid balance. Acute and chronic effects of hypoxia and their magnitude may differ and these will be highlighted. These changes will be related to the common diseases of high altitude and to their impact on patients with chronic renal disease. Other features of high altitude separate from hypoxia, either alone or in combination, including hypobaria, exercise, and cold may also signifi cantly perturb renal function.

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Section: Natriuretic Peptidesmentioning

confidence: 77%

Renal Function and Fluid Homeostasis

Swenson

Olsen

2013

High Altitude

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“…Relative hypoxaemia also stimulates myocardial angiogenesis and arterial and ventricular remodelling and enhances the contractile functional reserve of the myocardium 28 29 33. Most likely, these adaptations already occur at moderate altitudes 27 34. Many of the physiological adaptations are specific to the heart, which could explain that the associations of environmental exposures were stronger for IHD than for stroke 5 6.…”

Section: Discussionmentioning

confidence: 99%

Independent at heart: persistent association of altitude with ischaemic heart disease mortality after consideration of climate, topography and built environment

Faeh

Moser

Panczak

et al. 2016

J Epidemiol Community Health

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BACKGROUND: Living at higher altitude was dose-dependently associated with lower risk of ischaemic heart disease (IHD). Higher altitudes have different climatic, topographic and built environment properties than lowland regions. It is unclear whether these environmental factors mediate/confound the association between altitude and IHD. We examined how much of the altitude-IHD association is explained by variations in exposure at place of residence to sunshine, temperature, precipitation, aspect, slope and distance to main road. METHODS: We included 4.2 million individuals aged 40-84 at baseline living in Switzerland at altitudes 195-2971 m above sea level (ie, full range of residence), providing 77 127 IHD deaths. Mortality data 2000-2008, sociodemographic/economic information and coordinates of residence were obtained from the Swiss National Cohort, a longitudinal, census-based record linkage study. Environment information was modelled to residence level using Weibull regression models. RESULTS: In the model not adjusted for other environmental factors, IHD mortality linearly decreased with increasing altitude resulting in a lower risk (HR, 95% CI 0.67, 0.60 to 0.74) for those living >1500 m (vs<600 m). This association remained after adjustment for all other environmental factors 0.74 (0.66 to 0.82). CONCLUSIONS: The benefit of living at higher altitude was only partially confounded by variations in climate, topography and built environment. Rather, physical environment factors appear to have an independent effect and may impact on cardiovascular health in a cumulative way. Inclusion of additional modifiable factors as well as individual information on traditional IHD risk factors in our combined environmental model could help to identify strategies for the reduction of inequalities in IHD mortality. Independent at heart: Persistent association of altitude with ischemic heart disease mortality after consideration of climate, topography and built environment -a longitudinal cohort study ABSTRACTBackground Living at higher altitude was dose-dependently associated with lower risk of ischemic heart disease (IHD). Higher altitudes have different climatic, topographic and built environment properties than lowland regions. It is unclear whether these environmental factors mediate/confound the association between altitude and IHD. We examined how much of the altitude-IHD association is explained by variations in exposure at place of residence to sunshine, temperature, precipitation, aspect, slope and distance to main road.

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“…V O 2max at 4000 m. Altitude was simulated in a thermostabilized low-pressure chamber, equipped with a computerized altitude-controlling system (Koller et al 1993). The subject was under the supervision of a physician inside the chamber who was provided with an oxygen supply (Oxytron, Weinmann, Hamburg, Germany), and a physician outside the chamber.…”

Section: Methodsmentioning

confidence: 99%

Effects of hypobaric hypoxia on vascular endothelial growth factor and the acute phase response in subjects who are susceptible to high-altitude pulmonary oedema

Pavlíček¹,

Marti²,

Grad

et al. 2000

European Journal of Applied Physiology

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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 corresponding to 4000 m in a hypobaric chamber for 1 day. Peripheral venous blood was taken at 450 m (Zürich level) and at 4000 m, and levels of erythropoietin (EPO), VEGF, interleukin-6 (IL-6) and the acute-phase proteins complement C3 (C3), alpha1-antitrypsin (alpha1AT), transferrin (Tf) and C-reactive protein (CRP) were measured. Peripheral arterial oxygen saturation (SaO2) was recorded. Chest radiography was performed before and immediately after the experiment. EPO increased during altitude exposure, correlating with SaO2, in both groups (r = -0.86, P < 0.001). Venous serum VEGF did not show any elevation despite a marked decrease in SaO2 in the HAPE-S subjects [mean (SD) HAPE-S: 69.6 (9.1)%; controls: 78.7 (5.2)%]. C3 and alpha1AT levels increased in HAPE-S during hypobaric hypoxia [from 0.94 (0.11) g/l to 1.07 (0.13) g/l, and from 1.16 (0.08) g/l to 1.49 (0.27) g/l, respectively; P < 0.05], but remained within the clinical reference ranges. No significant elevations of IL-6, Tf or CRP were observed in either group. The post-exposure chest radiography revealed no signs of oedema. We conclude that VEGF is not up-regulated in HAPE-S and thus does not seem to increase critically pulmonary vascular permeability during the 1st day at high altitude. Furthermore, our data provide evidence against a clinically relevant inflammation in the initial phase of exposure to hypoxia in HAPE-S, although C3 and alpha1AT are mildly induced.

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The effects of acute altitude exposure in swiss highlanders and lowlanders

Cited by 16 publications

References 26 publications

Renal Function and Fluid Homeostasis

Renal Function and Fluid Homeostasis

Independent at heart: persistent association of altitude with ischaemic heart disease mortality after consideration of climate, topography and built environment

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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