Prediction of Susceptibility to Acute Mountain Sickness by SaO2 Values during Short-Term Exposure to Hypoxia

2004 ◽  
Vol 5 (3) ◽  
pp. 335-340 ◽  
Author(s):  
Martin Burtscher ◽  
Markus Flatz ◽  
Martin Faulhaber
Keyword(s):  
Acute Mountain Sickness ◽  
Short Term ◽  
Short Term Exposure ◽  
Mountain Sickness

scholarly journals Changes of Cerebral Blood Flow during Short-Term Exposure to Normobaric Hypoxia

1998 ◽  
Vol 18 (8) ◽  
pp. 906-910 ◽  
Author(s):  
Alfred Buck ◽  
Christian Schirlo ◽  
Valeska Jasinsky ◽  
Bruno Weber ◽  
Cyrill Burger ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Time Course ◽  
Acute Mountain Sickness ◽  
Statistical Parametric Mapping ◽  
Field Studies ◽  
Short Term ◽  
Positron Emission ◽  
Potential Association ◽  
Short Term Exposure

Decreased arterial partial oxygen pressure (PaO2) below a certain level presents a strong stimulus for increasing cerebral blood flow. Although several field studies examined the time course of global cerebral blood flow (gCBF) changes during hypoxia at high altitude, little was known about the regional differences in the flow pattern. Positron emission tomography (PET) with [15O]H2O was used on eight healthy volunteers to assess regional cerebral blood flow (rCBF) during short-term exposure to hypoxia corresponding to simulated altitudes of 3,000 and 4,500 m. Scans at the simulated altitudes were preceded and followed by baseline scans at the altitude of Zurich (450 m, baseline-1 and baseline-2). Each altitude stage lasted 20 minutes. From baseline to 4,500 m, gCBF increased from 34.4 ± 5.9 to 41.6 ± 9.0 mL · minute−1 · 100 g−1 (mean ± SD), whereas no significant change was noted at 3,000 m. During baseline-2 the flow values returned to those of baseline-1. Statistical parametric mapping identified the hypothalamus as the only region with excessively increased blood flow at 4,500 m (+32.8% ± 21.9% relative to baseline-1). The corresponding value for the thalamus, the structure with the second largest increase, was 19.2% ± 16.3%. Compared with the rest of the brain, an excessive increase of blood flow during acute exposure to hypoxia is found in the hypothalamus. The functional implications are at present unclear. Further studies of this finding should elucidate its meaning and especially focus on a potential association with the symptoms of acute mountain sickness.

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
Keyword(s):  
Physical Performance ◽  
Acute Mountain Sickness ◽  
Drug Dosage ◽  
Full Scale ◽  
Limiting Factors ◽  
Hypoxic Exposure ◽  
Short Term ◽  
Middle Mountains ◽  
Effective Doses ◽  
Mountain Sickness

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).

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.

Short-term intermittent hypoxia reduces the severity of acute mountain sickness

2012 ◽  
Vol 22 (5) ◽  
pp. e79-e85 ◽  
Author(s):  
M. Wille ◽  
H. Gatterer ◽  
K. Mairer ◽  
M. Philippe ◽  
H. Schwarzenbacher ◽  
...  
Keyword(s):  
Intermittent Hypoxia ◽  
Acute Mountain Sickness ◽  
Short Term ◽  
Mountain Sickness

scholarly journals Cerebral Hemodynamic and Ventilatory Responses to Hypoxia, Hypercapnia, and Hypocapnia during 5 Days at 4,350 m

2013 ◽  
Vol 34 (1) ◽  
pp. 52-60 ◽  
Author(s):  
Thomas Rupp ◽  
François Esteve ◽  
Pierre Bouzat ◽  
Carsten Lundby ◽  
Stéphane Perrey ◽  
...  
Keyword(s):  
Near Infrared ◽  
Cerebral Oxygenation ◽  
Acute Mountain Sickness ◽  
Oxygenation Index ◽  
Short Term ◽  
Ventilatory Responses ◽  
Altitude Exposure ◽  
Total Hemoglobin ◽  
Tissue Oxygenation Index ◽  
Mountain Sickness

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.

The Effect of Dimethyl Sulfoxide on In Vitro Platelet Function

1976 ◽  
Vol 36 (01) ◽  
pp. 221-229 ◽  
Author(s):  
Charles A. Schiffer ◽  
Caroline L. Whitaker ◽  
Morton Schmukler ◽  
Joseph Aisner ◽  
Steven L. Hilbert
Keyword(s):  
Platelet Count ◽  
Platelet Aggregation ◽  
Dimethyl Sulfoxide ◽  
Platelet Function ◽  
Platelet Volume ◽  
Short Term ◽  
Platelet Factor ◽  
Short Term Exposure ◽  
Structural Abnormalities

SummaryAlthough dimethyl sulfoxide (DMSO) has been used extensively as a cryopreservative for platelets there are few studies dealing with the effect of DMSO on platelet function. Using techniques similar to those employed in platelet cryopreservation platelets were incubated with final concentrations of 2-10% DMSO at 25° C. After exposure to 5 and 10% DMSO platelets remained discoid and electron micrographs revealed no structural abnormalities. There was no significant change in platelet count. In terms of injury to platelet membranes, there was no increased availability of platelet factor-3 or leakage of nucleotides, 5 hydroxytryptamine (5HT) or glycosidases with final DMSO concentrations of 2.5, 5 and 10% DMSO. Thrombin stimulated nucleotide and 5HT release was reduced by 10% DMSO. Impairment of thrombin induced glycosidase release was noted at lower DMSO concentrations and was dose related. Similarly, aggregation to ADP was progressively impaired at DMSO concentrations from 1-5% and was dose related. After the platelets exposed to DMSO were washed, however, aggregation and release returned to control values. Platelet aggregation by epinephrine was also inhibited by DMSO and this could not be corrected by washing the platelets. DMSO-plasma solutions are hypertonic but only minimal increases in platelet volume (at 10% DMSO) could be detected. Shrinkage of platelets was seen with hypertonic solutions of sodium chloride or sucrose suggesting that the rapid transmembrane passage of DMSO prevented significant shifts of water. These studies demonstrate that there are minimal irreversible alterations in in vitro platelet function after short-term exposure to DMSO.

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