scholarly journals The administration of acetazolamidum for the symptom prophylaxis of an acute mountain sickness when short-term dislocation from middle mountains to highlands takes place

2018 ◽  
Vol 16 (2) ◽  
pp. 42-48
Author(s):  
Oleg V Vetryakov ◽  
Vladimir N Bykov ◽  
Ivan V Fateev ◽  
Yuriy Sh Khalimov

The development of mountain sickness symptoms is one of the limiting factors of successful physical performance in middle mountains and highlands. Among drugs with established effectiveness for the prophylaxis of an acute mountain sickness carbonic anhydrase inhibitor acetazolamidum is also viewed, but at presence there is no universal approach to this issue and drug dosage regimen for its administration have not been elaborated. Aim. А comprehensive analysis of acetazolamidum being administered in the range of effective doses has been carried out. Methods. During the experiment the effect of acetazolamidum on physical performance and resistance of rats to an acute hypobaric hypoxia when administered in the range of effective doses (20, 40 and 80 mg/kg) was studied. During full-scale approbation the effect of acetazolamidum in various dosages on adaptation processes in the course of a rapid dislocation from middle mountains to highlands (glade Azau-the Elbrus mountain) was assessed. Results. The undertaken study showed that the administration of acetazolamidum to rats beginning from a daily dosage 20 mg/kg, that corresponds to human intake of 250 mg of the drug, promotes significant increase of survival time of rats following acute hypoxic exposure as well as growth of an animal performance ability factor under hypoxia. Conclusion. In the course of full-scale approbation it was established that prophylactic intake of acetazolamidum in examined doses prevents the development of symptoms of an acute mountain sickness when rapid dislocation from middle mountains (2300 m) to highlands (5000 m) takes place in the background of physical activity according to the results of sportsmen’s performance of Lake Louise test. (For citation: Vetryakov OV, Bykov VN, Fateev IV, Khalimov YS. The administration of acetazolamidum for the symptom prophylaxis of an acute mountain sickness when short-term dislocation from middle mountains to highlands takes place. Reviews on Clinical Pharmacology and Drug Therapy. 2018;16(2):42-48. doi: 10.17816/RCF16242-48).

2008 ◽  
Vol 40 (Supplement) ◽  
pp. S170-S171
Author(s):  
Ken Kambis ◽  
Julie Barnes ◽  
Michio Yasukawa ◽  
Reina Chamberlain ◽  
Tiffanie Tsui ◽  
...  

2014 ◽  
Vol 116 (7) ◽  
pp. 945-952 ◽  
Author(s):  
Normand A. Richard ◽  
Inderjeet S. Sahota ◽  
Nadia Widmer ◽  
Sherri Ferguson ◽  
A. William Sheel ◽  
...  

We examined the control of breathing, cardiorespiratory effects, and the incidence of acute mountain sickness (AMS) in humans exposed to hypobaric hypoxia (HH) and normobaric hypoxia (NH), and under two control conditions [hypobaric normoxia (HN) and normobaric normoxia (NN)]. Exposures were 6 h in duration, and separated by 2 wk between hypoxic exposures and 1 wk between normoxic exposures. Before and after exposures, subjects ( n = 11) underwent hyperoxic and hypoxic Duffin CO2 rebreathing tests and a hypoxic ventilatory response test (HVR). Inside the environmental chamber, minute ventilation (V̇e), tidal volume (Vt), frequency of breathing ( fB), blood oxygenation, heart rate, and blood pressure were measured at 5 and 30 min and hourly until exit. Symptoms of AMS were evaluated using the Lake Louise score (LLS). Both the hyperoxic and hypoxic CO2 thresholds were lower after HH and NH, whereas CO2 sensitivity was increased after HH and NH in the hypoxic test and after NH in the hyperoxic test. Values for HVR were similar across the four exposures. No major differences were observed for V̇e or any other cardiorespiratory variables between NH and HH. The LLS was greater in AMS-susceptible than in AMS-resistant subjects; however, LLS was alike between HH and NH. In AMS-susceptible subjects, fB correlated positively and Vt negatively with the LLS. We conclude that 6 h of hypoxic exposure is sufficient to lower the peripheral and central CO2 threshold but does not induce differences in cardiorespiratory variables or AMS incidence between HH and NH.


2018 ◽  
Vol 3 (3) ◽  
pp. 209 ◽  
Author(s):  
Gopinath Bhaumik ◽  
Deepak Dass ◽  
Dishari Ghosh ◽  
Harish Kumar ◽  
Sanjiva Kumar ◽  
...  

<p>In emergencies/war like situations, rapid deployment of army personnel into high altitude occurs without proper acclimatization. Rapid deployment of unacclimatized soldiers to high mountainous environments may cause debilitating effects on operational capabilities and development of acute mountain sickness (AMS). Altitude acclimatization is the best strategy for the prevention of AMS Use of pharmacological intervention for prevention of AMS is a common practice. The use of intermittent hypoxic exposure (IHE) is an alternative approach for altitude acclimatization and it reduces occurrence and severity of AMS is. But, the use of intermittent normobaric hypoxia exposure at sea level on occurrence of AMS after acute ascent to 3500m altitude in Indian army personnel has not been tested yet.<strong></strong></p>


2005 ◽  
Vol 289 (6) ◽  
pp. H2364-H2372 ◽  
Author(s):  
Paola A. Lanfranchi ◽  
Roberto Colombo ◽  
George Cremona ◽  
Paolo Baderna ◽  
Liliana Spagnolatti ◽  
...  

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.


2012 ◽  
Vol 22 (5) ◽  
pp. e79-e85 ◽  
Author(s):  
M. Wille ◽  
H. Gatterer ◽  
K. Mairer ◽  
M. Philippe ◽  
H. Schwarzenbacher ◽  
...  

2013 ◽  
Vol 34 (1) ◽  
pp. 52-60 ◽  
Author(s):  
Thomas Rupp ◽  
François Esteve ◽  
Pierre Bouzat ◽  
Carsten Lundby ◽  
Stéphane Perrey ◽  
...  

This study investigated the changes in cerebral near-infrared spectroscopy (NIRS) signals, cerebrovascular and ventilatory responses to hypoxia and CO2 during altitude exposure. At sea level (SL), after 24 hours and 5 days at 4,350 m, 11 healthy subjects were exposed to normoxia, isocapnic hypoxia, hypercapnia, and hypocapnia. The following parameters were measured: prefrontal tissue oxygenation index (TOI), oxy- (HbO2), deoxy- and total hemoglobin (HbTot) concentrations with NIRS, blood velocity in the middle cerebral artery (MCAv) with transcranial Doppler and ventilation. Smaller prefrontal deoxygenation and larger ΔHbTot in response to hypoxia were observed at altitude compared with SL (day 5: ΔHbO2−0.6±1.1 versus −1.8±1.3  μmol/cmper mm Hg and ΔHbTot 1.4±1.3 versus 0.7±1.1  μmol/cm per mm Hg). The hypoxic MCAv and ventilatory responses were enhanced at altitude. Prefrontal oxygenation increased less in response to hypercapnia at altitude compared with SL (day 5: ΔTOI 0.3±0.2 versus 0.5±0.3% mm Hg). The hypercapnic MCAv and ventilatory responses were decreased and increased, respectively, at altitude. Hemodynamic responses to hypocapnia did not change at altitude. Short-term altitude exposure improves cerebral oxygenation in response to hypoxia but decreases it during hypercapnia. Although these changes may be relevant for conditions such as exercise or sleep at altitude, they were not associated with symptoms of acute mountain sickness.


2011 ◽  
Vol 111 (2) ◽  
pp. 392-399 ◽  
Author(s):  
Colleen Glyde Julian ◽  
Andrew W. Subudhi ◽  
Megan J. Wilson ◽  
Andrew C. Dimmen ◽  
Travis Pecha ◽  
...  

The pathophysiology of acute mountain sickness (AMS) is unknown. One hypothesis is that hypoxia induces biochemical changes that disrupt the blood-brain barrier (BBB) and, subsequently, lead to the development of cerebral edema and the defining symptoms of AMS. This study explores the relationship between AMS and biomarkers thought to protect against or contribute to BBB disruption. Twenty healthy volunteers participated in a series of hypobaric hypoxia trials distinguished by pretreatment with placebo, acetazolamide (250 mg), or dexamethasone (4 mg), administered using a randomized, double-blind, placebo-controlled, crossover design. Each trial included peripheral blood sampling and AMS assessment before (−15 and 0 h) and during (0.5, 4, and 9 h) a 10-h hypoxic exposure (barometric pressure = 425 mmHg). Anti-inflammatory and/or anti-permeability [interleukin (IL)-1 receptor agonist (IL-1RA), heat shock protein (HSP)-70, and adrenomedullin], proinflammatory (IL-6, IL-8, IL-2, IL-1β, and substance P), angiogenic, or chemotactic biomarkers (macrophage inflammatory protein-1β, VEGF, TNF-α, monocyte chemotactic protein-1, and matrix metalloproteinase-9) were assessed. AMS-resistant subjects had higher IL-1RA (4 and 9 h and overall), HSP-70 (0 h and overall), and adrenomedullin (overall) compared with AMS-susceptible subjects. Acetazolamide raised IL-1RA and HSP-70 compared with placebo in AMS-susceptible subjects. Dexamethasone also increased HSP-70 and adrenomedullin in AMS-susceptible subjects. Macrophage inflammatory protein-1β was higher in AMS-susceptible than AMS-resistant subjects after 4 h of hypoxia; dexamethasone minimized this difference. Other biomarkers were unrelated to AMS. Resistance to AMS was accompanied by a marked anti-inflammatory and/or anti-permeability response that may have prevented downstream pathophysiological events leading to AMS. Conversely, AMS susceptibility does not appear to be related to an exaggerated inflammatory response.


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