scholarly journals Relationship between Changes in Cerebral Blood Flow with Symptoms of Acute Mountain Sickness in Men Repeatedly Exposed to Simulated High Altitude

2017 ◽  
Vol 07 (01) ◽  
pp. 49-59
Author(s):  
Peter Ondruš ◽  
Roman Alberty ◽  
Timothy Lyons ◽  
Stephen Muza ◽  
Vincent Echavé ◽  
...  
2004 ◽  
Vol 106 (3) ◽  
pp. 279-285 ◽  
Author(s):  
Christopher LYSAKOWSKI ◽  
Erik VON ELM ◽  
Lionel DUMONT ◽  
Jean-Daniel JUNOD ◽  
Edömer TASSONYI ◽  
...  

Cerebral blood flow is thought to increase at high altitude and in subjects suffering from acute mountain sickness (AMS); however, data from the literature are contentious. Blood flow velocity in the middle cerebral artery (MCAv) may be used as a proxy measure of cerebral blood flow. Using transcranial Doppler sonography, MCAv was measured during normo- and hyper-ventilation in subjects who participated in a trial that tested the effect of magnesium supplementation on the prevention of AMS. First, MCAv was recorded at 353 m (baseline). Subjects were then randomized to receive oral magnesium citrate and matching placebo. A second measurement was taken after a 24±2 h ascent from 1130 m to 4559 m (altitude I), and a third after a 20–24 h stay at 4559 m (altitude II). Using multivariate linear regression, an association was sought between MCAv and magnesium supplementation, subjects′ age and gender, altitude itself, a temporary stay at altitude, and the presence of AMS (Lake Louise Score >6 with ataxia, nausea and/or headache). Subjects with AMS had additional Doppler recordings immediately before and after rescue medication (oxygen, dexamethasone and acetazolamide). Forty-seven subjects had measurements at baseline, 39 (21 receiving magnesium and 18 placebo) at altitude I and 26 (13 receiving magnesium and 13 placebo) at altitude II. During hyperventilation, MCAv decreased consistently (for each measurement, P<0.001). Magnesium significantly increased MCAv by 8.4 cm·s-1 (95% confidence interval, 1.8–15), but did not prevent AMS. No other factors were associated with MCAv. Eleven subjects had severe AMS [median score (range), 11 (8–16)] and, after rescue medication, the median score decreased to 3 (range, 0–5; P=0.001), but MCAv remained unchanged (65±18 cm·s-1 before compared with 67±16 cm·s-1 after rescue medication; P=0.79). MCAv was increased in subjects who received magnesium, but was not affected by exposure to high altitude or by severe AMS.


1989 ◽  
Vol 8 (3) ◽  
pp. 143-148 ◽  
Author(s):  
S M Otis ◽  
M E Rossman ◽  
P A Schneider ◽  
M P Rush ◽  
E B Ringelstein

1988 ◽  
Vol 74 (s18) ◽  
pp. 1P-1P ◽  
Author(s):  
AD Wright ◽  
AR Bradwell ◽  
J Jensen ◽  
N Lassen

2013 ◽  
Vol 114 (1) ◽  
pp. 11-18 ◽  
Author(s):  
Zachary M. Smith ◽  
Erin Krizay ◽  
Jia Guo ◽  
David D. Shin ◽  
Miriam Scadeng ◽  
...  

Acute mountain sickness (AMS) is a common condition occurring within hours of rapid exposure to high altitude. Despite its frequent occurrence, the pathophysiological mechanisms that underlie the condition remain poorly understood. We investigated the role of cerebral oxygen metabolism (CMRO2) in AMS. The purpose of this study was to test 1) if CMRO2 changes in response to hypoxia, and 2) if there is a difference in how individuals adapt to oxygen metabolic changes that may determine who develops AMS and who does not. Twenty-six normal human subjects were recruited into two groups based on Lake Louise AMS score (LLS): those with no AMS (LLS ≤ 2), and those with unambiguous AMS (LLS ≥ 5). [Subjects with intermediate scores (LLS 3–4) were not included.] CMRO2 was calculated from cerebral blood flow and arterial-venous difference in O2 content. Cerebral blood flow was measured using arterial spin labeling MRI; venous O2 saturation was calculated from the MRI of transverse relaxation in the superior sagittal sinus. Arterial O2 saturation was measured via pulse oximeter. Measurements were made during normoxia and after 2-day high-altitude exposure at 3,800 m. In all subjects, CMRO2 increased with sustained high-altitude hypoxia [1.54 (0.37) to 1.82 (0.49) μmol·g−1·min−1, n = 26, P = 0.045]. There was no significant difference in CMRO2 between AMS and no-AMS groups. End-tidal Pco2 was significantly reduced during hypoxia. Low arterial Pco2 is known to increase neural excitability, and we hypothesize that the low arterial Pco2 resulting from ventilatory acclimatization causes the observed increase in CMRO2.


1999 ◽  
Vol 31 (Supplement) ◽  
pp. S182 ◽  
Author(s):  
R. C. Roach ◽  
D. Maes ◽  
D. Sandoval ◽  
R. A. Robergs ◽  
M. Icenogle ◽  
...  

2008 ◽  
Vol 160 (3) ◽  
pp. 267-276 ◽  
Author(s):  
Edward A.W. Dyer ◽  
Susan R. Hopkins ◽  
Joanna E. Perthen ◽  
Richard B. Buxton ◽  
David J. Dubowitz

2009 ◽  
Vol 106 (2) ◽  
pp. 454-460 ◽  
Author(s):  
Martina M. Bosch ◽  
Tobias M. Merz ◽  
Daniel Barthelmes ◽  
Benno L. Petrig ◽  
Frederic Truffer ◽  
...  

Little is known about the ocular and cerebral blood flow during exposure to increasingly hypoxic conditions at high altitudes. There is evidence that an increase in cerebral blood flow resulting from altered autoregulation constitutes a risk factor for acute mountain sickness (AMS) and high-altitude cerebral edema (HACE) by leading to capillary overperfusion and vasogenic cerebral edema. The retina represents the only part of the central nervous system where capillary blood flow is visible and can be measured by noninvasive means. In this study we aimed to gain insights into retinal and choroidal autoregulatory properties during hypoxia and to correlate circulatory changes to symptoms of AMS and clinical signs of HACE. This observational study was performed within the scope of a high-altitude medical research expedition to Mount Muztagh Ata (7,546 m). Twenty seven participants underwent general and ophthalmic examinations up to a maximal height of 6,800 m. Examinations included fundus photography and measurements of retinal and choroidal blood flow, as well as measurement of arterial oxygen saturation and hematocrit. The initial increase in retinal blood velocity was followed by a decrease despite further ascent, whereas choroidal flow increase occurred later, at even higher altitudes. The sum of all adaptational mechanisms resulted in a stable oxygen delivery to the retina and the choroid. Parameters reflecting the retinal circulation and optic disc swelling correlated well with the occurrence of AMS-related symptoms. We demonstrate that sojourns at high altitudes trigger distinct behavior of retinal and choroidal blood flow. Increase in retinal but not in choroidal blood flow correlated with the occurrence of AMS-related symptoms.


PLoS ONE ◽  
2012 ◽  
Vol 7 (11) ◽  
pp. e50334 ◽  
Author(s):  
Klemens Mairer ◽  
Markus Göbel ◽  
Michaela Defrancesco ◽  
Maria Wille ◽  
Hubert Messner ◽  
...  

1999 ◽  
Vol 86 (5) ◽  
pp. 1578-1582 ◽  
Author(s):  
Ralf W. Baumgartner ◽  
Ioakim Spyridopoulos ◽  
Peter Bärtsch ◽  
Marco Maggiorini ◽  
Oswald Oelz

To evaluate the pathogenetic role of cerebral blood flow (CBF) changes occurring before and during the development of acute mountain sickness (AMS), peak mean middle cerebral artery flow velocities ([Formula: see text]) were assessed by transcranial Doppler sonography in 10 subjects at 490-m altitude, and during three 12-min periods immediately (SA1), 3 (SA2), and 6 (SA3) h after decompression to a simulated altitude of 4,559 m. AMS cerebral scores increased from 0.16 ± 0.14 at baseline to 0.44 ± 0.31 at SA1, 1.11 ± 0.88 at SA2( P < 0.05), and 1.43 ± 1.03 at SA3( P < 0.01); correspondingly, three, seven, and eight subjects had AMS. Absolute and relative[Formula: see text] at simulated altitude, expressed as percentages of low-altitude values (%[Formula: see text]), did not correlate with AMS cerebral scores. Average %[Formula: see text] remained unchanged, because %[Formula: see text]increased in three and remained unchanged or decreased in seven subjects at SA2 and SA3. These results suggest that CBF is not important in the pathogenesis of AMS and shows substantial interindividual differences during the first hours at simulated altitude.


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