scholarly journals Remote ischemic preconditioning does not prevent acute mountain sickness after rapid ascent to 3,450 m

2017 ◽  
Vol 123 (5) ◽  
pp. 1228-1234 ◽  
Author(s):  
Marc M. Berger ◽  
Franziska Macholz ◽  
Lukas Lehmann ◽  
Daniel Dankl ◽  
Marcel Hochreiter ◽  
...  
Keyword(s):  
Pulmonary Hypertension ◽  
High Altitude ◽  
Ischemic Preconditioning ◽  
Acute Mountain Sickness ◽  
Remote Ischemic Preconditioning ◽  
Systolic Pulmonary Artery Pressure ◽  
Transthoracic Doppler Echocardiography ◽  
Rapid Ascent ◽  
Mountain Sickness ◽  
The Brain

Remote ischemic preconditioning (RIPC) has been shown to protect remote organs, such as the brain and the lung, from damage induced by subsequent hypoxia or ischemia. Acute mountain sickness (AMS) is a syndrome of nonspecific neurologic symptoms and in high-altitude pulmonary edema excessive hypoxic pulmonary vasoconstriction (HPV) plays a pivotal role. We hypothesized that RIPC protects the brain from AMS and attenuates the magnitude of HPV after rapid ascent to 3,450 m. Forty nonacclimatized volunteers were randomized into two groups. At low altitude (750 m) the RIPC group ( n = 20) underwent 4 × 5 min of lower-limb ischemia (induced by inflation of bilateral thigh cuffs to 200 mmHg) followed by 5 min of reperfusion. The control group ( n = 20) underwent a sham protocol (4 × 5 min of bilateral thigh cuff inflation to 20 mmHg). Thereafter, participants ascended to 3,450 m by train over 2 h and stayed there for 48 h. AMS was evaluated by the Lake Louise score (LLS) and the AMS-C score. Systolic pulmonary artery pressure (SPAP) was assessed by transthoracic Doppler echocardiography. RIPC had no effect on the overall incidence (RIPC: 35%, control: 35%, P = 1.0) and severity (RIPC vs. control: P = 0.496 for LLS; P = 0.320 for AMS-C score) of AMS. RIPC also had no significant effect on SPAP [maximum after 10 h at high altitude; RIPC: 33 (SD 8) mmHg; controls: 37 (SD 7) mmHg; P = 0.19]. This study indicates that RIPC, performed immediately before passive ascent to 3,450 m, does not attenuate AMS and the magnitude of high-altitude pulmonary hypertension. NEW & NOTEWORTHY Remote ischemic preconditioning (RIPC) has been reported to improve neurologic and pulmonary outcome following an acute ischemic or hypoxic insult, yet the effect of RIPC for protecting from high-altitude diseases remains to be determined. The present study shows that RIPC, performed immediately before passive ascent to 3,450 m, does not attenuate acute mountain sickness and the degree of high-altitude pulmonary hypertension. Therefore, RIPC cannot be recommended for prevention of high-altitude diseases.

Abstract 14359: Single Nucleotide Polymorphisms in Genes Involved in L-arginine / Dimethylarginine Metabolism Predispose for Pulmonary Hypertension and Acute Mountain Sickness at High Altitude

Circulation ◽  
2020 ◽  
Vol 142 (Suppl_3) ◽  
Author(s):  
Juliane Hannemann ◽  
Julia Zummack ◽  
PATRICIA SIQUES ◽  
JULIO BRITO ◽  
Rainer Boeger
Keyword(s):  
Pulmonary Hypertension ◽  
Relative Risk ◽  
Genetic Variability ◽  
High Altitude ◽  
Acute Mountain Sickness ◽  
Minor Allele ◽  
Nucleotide Polymorphisms ◽  
Single Nucleotide ◽  
Mountain Sickness ◽  
Study Participants

Introduction: Chronic (CH) and chronic-intermittent (CIH) exposure to hypoxia at high altitude causes acute or chronic mountain sickness and elevation of mean pulmonary arterial pressure (mPAP). This is paralleled by increased plasma levels of ADMA, an endogenous inhibitor of NO synthesis. ADMA is cleaved by dimethylarginine dimethylaminohydrolase (DDAH1 and DDAH2), whilst symmetric dimethylarginine (SDMA) is cleaved by AGXT2. Arginase (ARG1 and ARG2) competes with endothelial NO synthase (NOS3) for L-arginine as substrate. We have shown previously that baseline ADMA (at sea level) determines mPAP after six months of CIH; cut-off values of 25 mm Hg and 30 mm Hg are being used to diagnose high altitude pulmonary hypertension. Hypothesis: We hypothesized that genetic variability in genes coding for core enzymes of ADMA, SDMA, and L-arginine metabolism may predispose individuals for high altitude disease and pulmonary hypertension. Methods: We genotyped 16 common single nucleotide polymorphisms in the NOS3, DDAH1, DDAH2, AGXT2, ARG1 and ARG2 genes of 69 healthy male Chilean subjects. Study participants adhered to a CIH regimen (5d at 3,550m, 2d at sea level) for six months. Metabolites were measured by LC-MS/MS; mPAP was estimated by echocardiography at six months, and altitude acclimatization was assessed by Lake Louise Score and arterial oxygen saturation. Results: Carriers of the minor allele of DDAH1 rs233112 had a higher mean baseline ADMA level (0.76±0.03 vs. 0.67±0.02 μmol/l; p<0.05), whilst the major allele of DDAH2 rs805304 was linked to an exacerbated increase of ADMA in hypoxia (0.10±0.03 vs. 0.04±0.04 μmol/l; p<0.02). Study participants carrying the minor allele of ARG1 rs2781667 had a relative risk of elevated mPAP (>25 mm Hg) of 1.70 (1.56-1.85; p<0.0001), and carriers of the minor allele of NOS3 rs2070744 had a relative risk of elevated mPAP (>30 mm Hg) of 1.58 (1.47-1.69; p<0.0001). The NOS3 and DDAH2 genes were associated with the incidence of acute mountain sickness. Conclusions: We conclude that genetic variability in the L-arginine / ADMA / NO pathway is an important determinant of high altitude pulmonary hypertension and acute mountain sickness. DDAH1 is linked to baseline ADMA, whilst DDAH2 determines the response of ADMA to hypoxia.

Intracranial Pressure at High Altitude and Acute Mountain Sickness

1995 ◽  
Vol 89 (2) ◽  
pp. 201-204 ◽  
Author(s):  
A. D. Wright ◽  
C. H. E. Imray ◽  
M. S. C. Morrissey ◽  
R. J. Marchbanks ◽  
A. R. Bradwell
Keyword(s):  
Intracranial Pressure ◽  
High Altitude ◽  
Acute Hypoxia ◽  
Acute Mountain Sickness ◽  
Raised Intracranial Pressure ◽  
Rapid Ascent ◽  
Mountain Sickness ◽  
Pressure Changes ◽  
Serial Measurements

1. Raised intracranial pressure has been noted in severe forms of acute mountain sickness and high-altitude cerebral oedema, but the role of intracranial pressure in the pathogenesis of mild to moderate acute mountain sickness is unknown. 2. Serial measurements of intracranial pressure were made indirectly by assessing changes in tympanic membrane displacement in 24 healthy subjects on rapid ascent to 5200 m. 3. Acute hypoxia at 3440 m was associated with a rise in intracranial pressure, but no difference was found in pressure changes at 4120 or 5200 m in subjects with or without symptoms of acute mountain sickness. 4. Raised intracranial pressure, though temporarily associated with acute hypoxia, is not a feature of acute mountain sickness with mild or moderate symptoms.

scholarly journals Remote ischemic preconditioning delays the onset of acute mountain sickness in normobaric hypoxia

2015 ◽  
Vol 3 (3) ◽  
pp. e12325 ◽  
Author(s):  
Marc M. Berger ◽  
Hannah Köhne ◽  
Lorenz Hotz ◽  
Moritz Hammer ◽  
Kai Schommer ◽  
...  
Keyword(s):  
Ischemic Preconditioning ◽  
Acute Mountain Sickness ◽  
Normobaric Hypoxia ◽  
Remote Ischemic Preconditioning ◽  
Mountain Sickness

scholarly journals Acute mountain sickness (AMS) in a Nepali pilgrim after rapid ascent to a sacred lake (4380 m) in the Himalayas

2018 ◽  
Vol 11 (1) ◽  
pp. bcr-2017-222888
Author(s):  
Simant Singh Thapa ◽  
Buddha Basnyat
Keyword(s):  
High Altitude ◽  
Acute Mountain Sickness ◽  
Severe Headache ◽  
Vulnerable Group ◽  
High Incidence ◽  
The Usa ◽  
Rapid Ascent ◽  
Mountain Sickness ◽  
Supportive Management ◽  
Temporary Health

A 55-year-old female Nepali pilgrim presented to the Himalayan Rescue Association Temporary Health Camp near the sacred Gosainkund Lake (4380 m) north of Kathmandu, Nepal, with a complaint of severe headache, vomiting and light-headedness. She was diagnosed with severe acute mountain sickness. Intramuscular dexamethasone was administered. Paracetamol (acetaminophen in the USA and Canada) and ondansetron were given as supportive management for headache and nausea. Arrangements were made to have her carried down by a porter immediately. After the descent, all her symptoms resolved. High-altitude pilgrims are a more vulnerable group than trekkers and mountaineers. Pilgrims generally have a rapid ascent profile, have low awareness of altitude illness and are strongly motivated to gain religious merit by completing the pilgrimage. As a result, there is a high incidence of altitude illness among pilgrims travelling to high-altitude pilgrimage sites.

Intermittent Hypoxic Exposure Reduces Acute Mountain Sickness Upon Subsequent Rapid Ascent to High Altitude

2008 ◽  
Vol 40 (Supplement) ◽  
pp. S170-S171
Author(s):  
Ken Kambis ◽  
Julie Barnes ◽  
Michio Yasukawa ◽  
Reina Chamberlain ◽  
Tiffanie Tsui ◽  
...  
Keyword(s):  
High Altitude ◽  
Acute Mountain Sickness ◽  
Hypoxic Exposure ◽  
Rapid Ascent ◽  
Mountain Sickness

scholarly journals Involvement of overweight and lipid metabolism in the development of pulmonary hypertension under conditions of chronic intermittent hypoxia

2020 ◽  
Vol 10 (1_suppl) ◽  
pp. 42-49
Author(s):  
Patricia Siques ◽  
Julio Brito ◽  
Stefany Ordenes ◽  
Eduardo Pena
Keyword(s):  
Pulmonary Hypertension ◽  
Lipid Metabolism ◽  
High Altitude ◽  
Intermittent Hypoxia ◽  
Acute Mountain Sickness ◽  
Overweight And Obesity ◽  
Chronic Intermittent Hypoxia ◽  
Inflammatory Status ◽  
Mountain Sickness

There is growing evidence that exposure to hypoxia, regardless of the source, elicits several metabolic responses in individuals. These responses are constitutive and are usually observed under hypoxia but vary according to the type of exposure. The aim of this review was to describe the involvement of obesity and lipid metabolism in the development of high-altitude pulmonary hypertension and in the development of acute mountain sickness under chronic intermittent hypoxia. Overweight or obesity, which are common in individuals with long-term chronic intermittent hypoxia exposure (high-altitude miners, shift workers, and soldiers), are thought to play a major role in the development of acute mountain sickness and high-altitude pulmonary hypertension. This association may be rooted in the interactions between obesity-related metabolic and physical alterations, such as increased waist circumference and neck circumference, among others, which lead to critical ventilation impairments; these impairments aggravate hypoxemia at high altitude, thereby triggering high-altitude diseases. Overweight and obesity are strongly associated with higher mean pulmonary artery pressure in the context of long-term chronic intermittent hypoxia. Remarkably, de novo synthesis of triglycerides by the sterol regulatory element-binding protein-1c pathway has been demonstrated, mainly due to the upregulation of stearoyl-CoA desaturase-1, which is also associated with the same outcomes. Therefore, overweight, obesity, and other metabolic conditions may hinder proper acclimatization. The involved mechanisms include respiratory impairment, alteration of the nitric oxide pathways, inflammatory status, reactive oxygen species imbalance, and other metabolic changes; however, further studies are required.

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