Effect of high altitude and exercise on microvascular parameters in acclimatized subjects

2006 ◽  
Vol 110 (2) ◽  
pp. 207-215 ◽  
Author(s):  
Andreas Bauer ◽  
Florian Demetz ◽  
Dirk Bruegger ◽  
Martin Schmoelz ◽  
Sebastian Schroepfer ◽  
...  
Keyword(s):  
High Altitude ◽  
Hypobaric Hypoxia ◽  
Venous Pressure ◽  
Acute Mountain Sickness ◽  
White Blood Cells ◽  
Microvascular Permeability ◽  
Computer Assisted ◽  
Fluid Exchange ◽  
Equilibrium Pressure ◽  
Low Altitude

The role of microvascular fluid shifts in the adaptation to hypobaric hypoxia and its contribution to the pathophysiology of AMS (acute mountain sickness) is unresolved. In a systematic prospective study, we investigated the effects of hypobaric hypoxia and physical exercise alone, and in combination, on microvascular fluid exchange and related factors. We used computer-assisted VCP (venous congestion plethysmography) on the calves of ten altitude-acclimatized volunteers. We investigated the effects of: (i) actively climbing to an altitude of 3196 m, (ii) airlifting these subjects to the same altitude, and (iii) exercise at low altitude. CFC (capillary filtration capacity), Pvi (isovolumetric venous pressure) and Qa (calf blood flow) were assessed before and after each procedure and then repeated after an overnight rest. Measurements of CFC showed no evidence of increased microvascular permeability after any of the procedures. Pvi was significantly decreased (P<0.001) from 20.3±4.4 to 8.9±4.3 mmHg after active ascent, and was still significantly lower (P=0.009) after overnight rest at high altitude (13.6±5.9 mmHg). No such changes were observed after the passive ascent (16.7±4.0 mmHg at baseline; 17.3±4.5 mmHg after passive ascent; and 19.9±5.3 mmHg after overnight rest) or after exercise at low altitude. After the active ascent, Qa was significantly increased. We also found a significant correlation between Qa, Pvi and the number of circulating white blood cells. In conclusion, we found evidence to support the hypothesis that increased microvascular permeability associated with AMS does not occur in acclimatized subjects. We also observed that the microvascular equilibrium pressure (Pvi) fell in inverse relation to the increase in Qa, especially in hypoxic exercise. We hypothesize that this inverse relationship reflects the haemodynamic changes at the microvascular interface, possibly attributable to the flow-induced increases in endothelial surface shear forces.

Blood rheology in acute mountain sickness and high-altitude pulmonary edema

1991 ◽  
Vol 71 (3) ◽  
pp. 934-938 ◽  
Author(s):  
W. H. Reinhart ◽  
B. Kayser ◽  
A. Singh ◽  
U. Waber ◽  
O. Oelz ◽  
...  
Keyword(s):  
Pulmonary Edema ◽  
High Altitude ◽  
Acute Mountain Sickness ◽  
Blood Rheology ◽  
Plasma Viscosity ◽  
Erythrocyte Deformability ◽  
Erythrocyte Aggregation ◽  
High Altitude Pulmonary Edema ◽  
Mountain Sickness ◽  
Low Altitude

The role of blood rheology in the pathogenesis of acute mountain sickness and high-altitude pulmonary edema was investigated. Twenty-three volunteers, 12 with a history of high-altitude pulmonary edema, were studied at low altitude (490 m) and at 2 h and 18 h after arrival at 4,559 m. Eight subjects remained healthy, seven developed acute mountain sickness, and eight developed high-altitude pulmonary edema. Hematocrit, whole blood viscosity, plasma viscosity, erythrocyte aggregation, and erythrocyte deformability (filtration) were measured. Plasma viscosity and erythrocyte deformability remained unaffected. The hematocrit level was lower 2 h after the arrival at high altitude and higher after 18 h compared with low altitude. The whole blood viscosity changed accordingly. The erythrocyte aggregation was about doubled 18 h after the arrival compared with low-altitude values, which reflects the acute phase reaction. There were, however, no significant differences in any rheological parameters between healthy individuals and subjects with acute mountain sickness or high-altitude pulmonary edema, either before or during the illness. We conclude that rheological abnormalities can be excluded as an initiating event in the development of acute mountain sickness and high-altitude pulmonary edema.

Elevated plasma S100B levels in high altitude hypobaric hypoxia do not correlate with acute mountain sickness

2014 ◽  
Vol 36 (9) ◽  
pp. 779-785 ◽  
Author(s):  
Craig D. Winter ◽  
Timothy R. Whyte ◽  
John Cardinal ◽  
Stephen E. Rose ◽  
Peter K. O’Rourke ◽  
...  
Keyword(s):  
High Altitude ◽  
Hypobaric Hypoxia ◽  
Acute Mountain Sickness ◽  
Elevated Plasma ◽  
Mountain Sickness

Mountain neurology

2019 ◽  
Vol 19 (5) ◽  
pp. 404-411 ◽  
Author(s):  
Marieke Cornelia Johanna Dekker ◽  
Mark H Wilson ◽  
William Patrick Howlett
Keyword(s):  
High Altitude ◽  
Acute Mountain Sickness ◽  
Free Standing ◽  
Mount Kilimanjaro ◽  
Northern Tanzania ◽  
Neurological Conditions ◽  
Mountain Sickness ◽  
Low Altitude ◽  
Mountain Climbers ◽  
Altitude Illnesses

Mountain climbers may develop specific illnesses that largely depend on the altitude reached and the rate of ascent. The popularity of travel to high altitude destinations, extreme tourist activities and mountain climbing means that neurologists in low-altitude countries are increasingly likely to encounter neurological problems and disorders in people exposed to high altitude. Additionally, they may have to advise patients with pre-existing neurological conditions on the risks of ascent to altitude. This article focuses on neurological-related high-altitude illnesses: acute mountain sickness and high-altitude cerebral oedema, as well as high-altitude retinopathy and other neurological disorders. This overview combines current understood pathogenesis with the experience of managing altitude-related illness at the foot of Mount Kilimanjaro in northern Tanzania, the tallest free-standing mountain in the world.

scholarly journals Enhanced synthesis of albumin and fibrinogen at high altitude

2001 ◽  
Vol 90 (2) ◽  
pp. 528-537 ◽  
Author(s):  
Reinhard Imoberdorf ◽  
Peter J. Garlick ◽  
Margaret A. McNurlan ◽  
George A. Casella ◽  
Edgar Peheim ◽  
...  
Keyword(s):  
High Altitude ◽  
Hypobaric Hypoxia ◽  
Physical Exertion ◽  
Acute Effects ◽  
Albumin Synthesis ◽  
C Reactive Protein ◽  
Reactive Protein ◽  
Low Altitude ◽  
Made In ◽  
Stimulation Of

The acute effects of active and passive ascent to high altitude on plasma volume (PV) and rates of synthesis of albumin and fibrinogen have been examined. Measurements were made in two groups of healthy volunteers, initially at low altitude (550 m) and again on the day after ascent to high altitude (4,559 m). One group ascended by helicopter (air group, n = 8), whereas the other group climbed (foot group, n = 9), so that the separate contribution of physical exertion to the response could be delineated. PV was measured by dilution of125I-labeled albumin, whereas synthesis rates of albumin and fibrinogen were determined from the incorporation of isotope into protein after injection of [ ring-2H5]phenylalanine. In the air group, there was no change in PV at high altitude, whereas, in the foot group, there was a 10% increase in PV ( P < 0.01). Albumin synthesis (mg · kg−1· day−1) increased by 13% in the air group ( P = 0.058) and by 32% in the foot group ( P < 0.001). Fibrinogen synthesis (mg · kg−1· day−1) increased by 40% in the air group ( P = 0.068) and by 100% in the foot group ( P < 0.001). Hypoxia and alkalosis at high altitude did not differ between the groups. Plasma interleukin-6 was increased modestly in both groups but C-reactive protein was not changed in either group. It is concluded that increases in PV and plasma protein synthesis at high altitude result mainly from the physical exercise associated with climbing. However, a small stimulation of albumin and fibrinogen synthesis may be attributable to hypobaric hypoxia alone.

scholarly journals Greater free plasma VEGF and lower soluble VEGF receptor-1 in acute mountain sickness

2005 ◽  
Vol 98 (5) ◽  
pp. 1626-1629 ◽  
Author(s):  
Martha C. Tissot van Patot ◽  
Guy Leadbetter ◽  
Linda E. Keyes ◽  
Jamie Bendrick-Peart ◽  
Virginia E. Beckey ◽  
...  
Keyword(s):  
High Altitude ◽  
Acute Mountain Sickness ◽  
Significant Rise ◽  
Vegf Receptor ◽  
Vascular Endothelial ◽  
High Altitude Cerebral Edema ◽  
Mountain Sickness ◽  
Low Altitude ◽  
Endothelial Growth Factor ◽  
Free Plasma

Vascular endothelial growth factor (VEGF) is a hypoxia-induced protein that produces vascular permeability, and limited evidence suggests a possible role for VEGF in the pathophysiology of acute mountain sickness (AMS) and/or high-altitude cerebral edema (HACE). Previous studies demonstrated that plasma VEGF alone does not correlate with AMS; however, soluble VEGF receptor (sFlt-1), not accounted for in previous studies, can bind VEGF in the circulation, reducing VEGF activity. In the present study, we hypothesized that free VEGF is greater and sFlt-1 less in subjects with AMS compared with well individuals at high altitude. Subjects were exposed to 4,300 m for 19–20 h (baseline 1,600 m). The incidence of AMS was determined by using a modified Lake Louise symptom score and the Environmental Symptoms Questionnaire for cerebral effects. Plasma was collected at low altitude and after 24 h at high altitude, or at time of illness, and then analyzed by ELISA for VEGF and for soluble VEGF receptor, sFlt-1. AMS subjects had lower sFlt-1 at both low and high altitude compared with well subjects and a significant rise in free plasma VEGF on ascent to altitude compared with well subjects. We conclude that increased free plasma VEGF on ascent to altitude is associated with AMS and may play a role in pathophysiology of AMS.

Autonomic cardiovascular regulation in subjects with acute mountain sickness

2005 ◽  
Vol 289 (6) ◽  
pp. H2364-H2372 ◽  
Author(s):  
Paola A. Lanfranchi ◽  
Roberto Colombo ◽  
George Cremona ◽  
Paolo Baderna ◽  
Liliana Spagnolatti ◽  
...  
Keyword(s):  
High Altitude ◽  
Potential Role ◽  
Acute Mountain Sickness ◽  
Low Frequency ◽  
Short Term ◽  
Mountain Sickness ◽  
Low Altitude ◽  
Normalized Units ◽  
Hypoxic Gas Mixture

The aims of this study were 1) to evaluate whether subjects suffering from acute mountain sickness (AMS) during exposure to high altitude have signs of autonomic dysfunction and 2) to verify whether autonomic variables at low altitude may identify subjects who are prone to develop AMS. Forty-one mountaineers were studied at 4,559-m altitude. AMS was diagnosed using the Lake Louise score, and autonomic cardiovascular function was explored using spectral analysis of R-R interval and blood pressure (BP) variability on 10-min resting recordings. Seventeen subjects (41%) had AMS. Subjects with AMS were older than those without AMS ( P < 0.01). At high altitude, the low-frequency (LF) component of systolic BP variability (LFSBP) was higher ( P = 0.02) and the LF component of R-R variability in normalized units (LFRRNU) was lower ( P = 0.001) in subjects with AMS. After 3 mo, 21 subjects (43% with AMS) repeated the evaluation at low altitude at rest and in response to a hypoxic gas mixture. LFRRNU was similar in the two groups at baseline and during hypoxia at low altitude but increased only in subjects without AMS at high altitude ( P < 0.001) and did not change between low and high altitude in subjects with AMS. Conversely, LFSBP increased significantly during short-term hypoxia only in subjects with AMS, who also had higher resting BP ( P < 0.05) than those without AMS. Autonomic cardiovascular dysfunction accompanies AMS. Marked LFSBP response to short-term hypoxia identifies AMS-prone subjects, supporting the potential role of an exaggerated individual chemoreflex vasoconstrictive response to hypoxia in the genesis of AMS.

Depressed myocardial function in the goat at high altitude

1976 ◽  
Vol 41 (3) ◽  
pp. 356-361 ◽  
Author(s):  
C. E. Tucker ◽  
W. E. James ◽  
M. A. Berry ◽  
C. J. Johnstone ◽  
R. F. Grover
Keyword(s):  
High Altitude ◽  
Hypobaric Hypoxia ◽  
Chronic Hypoxia ◽  
Myocardial Function ◽  
Left Ventricular ◽  
Cardiac Performance ◽  
Left Ventricular Cavity ◽  
Wave Form ◽  
Low Altitude ◽  
The Relationship

To determine if depressed myocardial function contributes to the reported decrease in cardiac performance at high altitude, six chronically instrumented, unsedated goats were studied before, during, and after 2-wk exposureto hypobaric hypoxia (PaO2 44 mmHg). Undistorted ventricular pressure wave form was obtained from a miniature transducer implanted in the left ventricular cavity. The relationship between (dP/dt)/28P and P was extrapolated toobtain Vmax as an index of myocardial function. With beta sympathetic blockade (practolol) and pacing to reproduce heart rates, Vmax was uniformly andsignificantly depressed (P less than 0.01) during chronic hypoxia, and returned to control values following descent to low altitude. Likewise, stroke volume following saline infusion was decreased at high altitude and returned to control values following descent. Acute relief of hypoxia at high altitude by administration of 100% oxygen by mask did not reverse the depressedVmax. These findings indicate that chronic hypobaric hypoxia produces a depression of myocardial function which is reversible by chronic but not acuterelief of hypoxia.

scholarly journals Plasma Metabolomic Profiling of Individuals Susceptible to High Altitude through Gas Chromatograph- mass Spectrometry

2020 ◽  
Author(s):  
Chi Wang ◽  
Hui Jiang ◽  
Jingwen Chen ◽  
Jinyan Duan ◽  
Chengbin Wang
Keyword(s):  
Mass Spectrometry ◽  
High Altitude ◽  
Sea Level ◽  
Hypobaric Hypoxia ◽  
Acute Mountain Sickness ◽  
Principal Component ◽  
Gas Chromatography Mass Spectrometry ◽  
Pathophysiological Mechanism ◽  
Metabolomic Profiling ◽  
Gas Chromatograph Mass Spectrometry

Abstract Objective We aimed to characterize metabolic alterations of people ascending to high altitude and susceptible to acute mountain sickness (AMS). Methods Peripheral blood samples were collected from 36 healthy volunteers on the 3rd day ascending to high altitude (4300m). AMS status was assessed using the Lake Louise Questionnaire. Plasma samples were characterized by gas chromatography-mass spectrometry (GC-MS) and principal component analysis (PCA) was used to discriminate the metabolite changes between sea level and high altitude status and between AMS group and non-AMS group. Results High altitude hypobaric hypoxia caused significant and comprehensive metabolic changes in plasma, including 18 metabolites between sea level and high altitude, 6 metabolites between AMS group and non-AMS group. By using MetaboAnalyst 3.0, several key metabolic pathways were found to be involved, including cysteine and methionine metabolism, alanine, aspartate and glutamate metabolism. Conclusion The GC-MS profiling was a useful approach to analyze metabolites variances and provides potential targets for further investigation to understand the pathophysiological mechanism of hypobaric hypoxia and susceptibility to high altitude.

Flying, altitude, and diving

2021 ◽  
pp. 593-608
Author(s):  
Terry Robinson ◽  
Jane Scullion
Keyword(s):  
Lung Disease ◽  
High Altitude ◽  
Atmospheric Pressure ◽  
Hypobaric Hypoxia ◽  
Acute Mountain Sickness ◽  
Gas Composition ◽  
Gaseous Exchange ◽  
High Altitudes ◽  
Mountain Sickness

Up to an altitude of approximately 30,000 feet, the composition of the gas in the air we breathe remains almost constant. Atmospheric pressure decreases exponentially with altitude. This means that although the gas composition at high altitude remains the same, the air is less dense, resulting in less available oxygen for gaseous exchange. Hypobaric hypoxia therefore develops as a result of low atmospheric atmosphere. This chapter discusses the effects of flying, high altitudes, and diving on respiration. It starts by describing atmospheric pressure and altitude, the then-acute mountain sickness (AMS) and its management. Flying with lung disease is covered, alongside fitness to fly, the use of in-flight oxygen, and general precautions to take. Diving, diving-related illnesses, and practising the sport with pre-existing lung conditions are also included.

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