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.

scholarly journals Acute Mountain Sickness Following Incremental Trekking to High Altitude: Correlation With Plasma Vascular Endothelial Growth Factor Levels and the Possible Effects of Dexamethasone and Acclimatization Following Re-exposure

2021 ◽  
Vol 12 ◽  
Author(s):  
Craig Winter ◽  
Tracy Bjorkman ◽  
Stephanie Miller ◽  
Paul Nichols ◽  
John Cardinal ◽  
...  
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Growth Factor ◽  
High Altitude ◽  
Acute Mountain Sickness ◽  
Vascular Endothelial ◽  
Mountain Sickness ◽  
High Altitude Illness ◽  
Exercise Induced ◽  
Endothelial Growth Factor ◽  
Vegf Level

Purpose: The recognition and treatment of high-altitude illness (HAI) is increasingly important in global emergency medicine. High altitude related hypobaric hypoxia can lead to acute mountain sickness (AMS), which may relate to increased expression of vascular endothelial growth factor (VEGF), and subsequent blood-brain barrier (BBB) compromise. This study aimed to establish the relationship between AMS and changes in plasma VEGF levels during a high-altitude ascent. VEGF level changes with dexamethasone, a commonly used AMS medication, may provide additional insight into AMS.Methods: Twelve healthy volunteers ascended Mt Fuji (3,700 m) and blood samples were obtained at distinct altitudes for VEGF analysis. Oxygen saturation (SPO2) measurements were also documented at the same time-point. Six out of the 12 study participants were prescribed dexamethasone for a second ascent performed 48 h later, and blood was again collected to establish VEGF levels.Results: Four key VEGF observations could be made based on the data collected: (i) the baseline VEGF levels between the two ascents trended upwards; (ii) those deemed to have AMS in the first ascent had increased VEGF levels (23.8–30.3 pg/ml), which decreased otherwise (23.8–30.3 pg/ml); (iii) first ascent AMS participants had higher VEGF level variability for the second ascent, and similar to those not treated with dexamethasone; and (iv) for the second ascent dexamethasone participants had similar VEGF levels to non-AMS first ascent participants, and the variability was lower than for first ascent AMS and non-dexamethasone participants. SPO2 changes were unremarkable, other than reducing by around 5% irrespective of whether measurement was taken for the first or second ascent.Conclusion: First ascent findings suggest a hallmark of AMS could be elevated VEGF levels. The lack of an exercise-induced VEGF level change strengthened the notion that elevated plasma VEGF was brain-derived, and related to AMS.

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.

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 Cerebrovascular Dynamics and Vascular Endothelial Growth Factor in Acute Mountain Sickness

2006 ◽  
Vol 17 (1) ◽  
pp. 1-7 ◽  
Author(s):  
Joseph Palma ◽  
Christian Macedonia ◽  
Patricia Deuster ◽  
Cara Olsen ◽  
B. Robert Mozayeni ◽  
...  
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Growth Factor ◽  
Acute Mountain Sickness ◽  
Vascular Endothelial ◽  
Mountain Sickness ◽  
Endothelial Growth Factor

scholarly journals Acute Mountain Sickness, High Altitude Pulmonary Edema, and High Altitude Cerebral Edema: An enhanced view from the High Andes

2021 ◽  
Author(s):  
Gustavo Zubieta-Calleja ◽  
Natalia Zubieta-DeUrioste
Keyword(s):  
Pulmonary Edema ◽  
High Altitude ◽  
Cerebral Edema ◽  
Acute Mountain Sickness ◽  
Point Of View ◽  
La Paz ◽  
Mountain Climbing ◽  
High Altitude Pulmonary Edema ◽  
High Altitude Cerebral Edema ◽  
Mountain Sickness

Background: Travelling to high altitude for entertainment or work is sometimes associated with acute high altitude pathologies. In the past, scientific literature from the lowlander point of view was mostly based on mountain climbing. Nowadays, altitude descent and evacuation are not mandatory in populated highland cities. Methods: We present how to diagnose and treat acute high altitude pathologies based on 50 years of high altitude physiology and medical practice in hypobaric hypoxic diseases in La Paz, Bolivia (3,600m; 11,811ft), at the High Altitude Pulmonary and Pathology Institute (HAPPI – IPPA) altitudeclinic.com.Results: Acute Mountain Sickness, High Altitude Pulmonary Edema, and High Altitude Cerebral Edema are all medical conditions faced by some travelers. These can occasionally present after flights to high altitude cities, both in lowlanders or high-altitude residents during re-entry, particularly after spending more than 20 days at sea level.Conclusions: Acute high altitude ascent diseases can be adequately diagnosed and treated without altitude descent. Traveling to high altitude should not be feared as it has many benefits;

scholarly journals Acute Mountain Sickness, High Altitude Pulmonary Edema, and High Altitude Cerebral Edema: A view from the High Andes

2021 ◽  
Author(s):  
Gustavo Zubieta-Calleja ◽  
Natalia Zubieta-DeUrioste
Keyword(s):  
Pulmonary Edema ◽  
High Altitude ◽  
Cerebral Edema ◽  
Acute Mountain Sickness ◽  
Healthy Children ◽  
Number Of Children ◽  
High Altitude Pulmonary Edema ◽  
High Altitude Cerebral Edema ◽  
Potential Risks ◽  
Mountain Sickness

Healthy children and those with pre-existing conditions traveling to high altitude may experience diverse physiologic changes. Individuals who are not acclimatized and ascend rapidly are at risk of developing acute high altitude illnesses (HAI), which may occur within a few hours after arrival at high altitudes, being acute mountain sickness (AMS) the most common. In very few cases, serious complications may occur, including High Altitude Pulmonary Edema (HAPE) and very rarely High Altitude Cerebral Edema (HACE). Moreover, the number of children and adolescents traveling on commercial aircrafts is growing and this poses a need for their treating physicians to be aware of the potential risks of hypoxia while air traveling. In this article we present 50 years of medical practice at high altitude treating these pathologies succesfully with no casualties.

Rat brain VEGF expression in alveolar hypoxia: possible role in high-altitude cerebral edema

1998 ◽  
Vol 85 (1) ◽  
pp. 53-57 ◽  
Author(s):  
Fengping Xu ◽  
John W. Severinghaus
Keyword(s):  
High Altitude ◽  
Cerebral Edema ◽  
Northern Blot Analysis ◽  
Capillary Permeability ◽  
Vascular Endothelial ◽  
Vegf Expression ◽  
Vegf Mrna ◽  
High Altitude Cerebral Edema ◽  
Alveolar Hypoxia ◽  
Endothelial Growth Factor

The mechanism by which hypoxia causes high-altitude cerebral edema (HACE) is unknown. Tissue hypoxia triggers angiogenesis, initially by expressing vascular endothelial growth factor (VEGF), which has been shown to increase extracerebral capillary permeability. This study investigated brain VEGF expression in 32 rats exposed to progressively severe normobaric hypoxia (9–6% O2) for 0 (control), 3, 6, or 12 h or 1, 2, 3, or 6 days. O2concentration was adjusted intermittently to the limit of tolerance by activity and intake, but no attempt was made to detect HACE. Northern blot analysis demonstrated that two molecular bands of transcribed VEGF mRNA (∼3.9 and 4.7 kb) were upregulated in cortex and cerebellum after as little as 3 h of hypoxia, with a threefold increase peaking at 12–24 h. Western blot revealed that VEGF protein was increased after 12 h of hypoxia, reaching a maximum in ∼2 days. The expression of flt-1 mRNA was enhanced after 3 days of hypoxia. We conclude that VEGF production in hypoxia is consistent with the hypothesis that angiogenesis may be involved in HACE.

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