Effect of magnesium, high altitude and acute mountain sickness on blood flow velocity in the middle cerebral artery

2004 ◽  
Vol 106 (3) ◽  
pp. 279-285 ◽  
Author(s):  
Christopher LYSAKOWSKI ◽  
Erik VON ELM ◽  
Lionel DUMONT ◽  
Jean-Daniel JUNOD ◽  
Edömer TASSONYI ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Middle Cerebral Artery ◽  
High Altitude ◽  
Blood Flow Velocity ◽  
Rescue Medication ◽  
Acute Mountain Sickness ◽  
Median Score ◽  
Magnesium Supplementation ◽  
Mountain Sickness

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.

Relationship of cerebral blood flow regulation to acute mountain sickness.

1989 ◽  
Vol 8 (3) ◽  
pp. 143-148 ◽  
Author(s):  
S M Otis ◽  
M E Rossman ◽  
P A Schneider ◽  
M P Rush ◽  
E B Ringelstein
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Acute Mountain Sickness ◽  
Flow Regulation ◽  
Blood Flow Regulation ◽  
Mountain Sickness ◽  
Relationship Of

Direct Cerebral Vasodilatory Effects of Sevoflurane and Isoflurane 

1999 ◽  
Vol 91 (3) ◽  
pp. 677-677 ◽  
Author(s):  
Basil F. Matta ◽  
Karen J. Heath ◽  
Kate Tipping ◽  
Andrew C. Summors
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Middle Cerebral Artery ◽  
Flow Velocity ◽  
Cerebral Artery ◽  
Blood Flow Velocity ◽  
End Tidal

Background The effect of volatile anesthetics on cerebral blood flow depends on the balance between the indirect vasoconstrictive action secondary to flow-metabolism coupling and the agent's intrinsic vasodilatory action. This study compared the direct cerebral vasodilatory actions of 0.5 and 1.5 minimum alveolar concentration (MAC) sevoflurane and isoflurane during an propofol-induced isoelectric electroencephalogram. Methods Twenty patients aged 20-62 yr with American Society of Anesthesiologists physical status I or II requiring general anesthesia for routine spinal surgery were recruited. In addition to routine monitoring, a transcranial Doppler ultrasound was used to measure blood flow velocity in the middle cerebral artery, and an electroencephalograph to measure brain electrical activity. Anesthesia was induced with propofol 2.5 mg/kg, fentanyl 2 micro/g/kg, and atracurium 0.5 mg/kg, and a propofol infusion was used to achieve electroencephalographic isoelectricity. End-tidal carbon dioxide, blood pressure, and temperature were maintained constant throughout the study period. Cerebral blood flow velocity, mean blood pressure, and heart rate were recorded after 20 min of isoelectric encephalogram. Patients were then assigned to receive either age-adjusted 0.5 MAC (0.8-1%) or 1.5 MAC (2.4-3%) end-tidal sevoflurane; or age-adjusted 0.5 MAC (0.5-0.7%) or 1.5 MAC (1.5-2%) end-tidal isoflurane. After 15 min of unchanged end-tidal concentration, the variables were measured again. The concentration of the inhalational agent was increased or decreased as appropriate, and all measurements were repeated again. All measurements were performed before the start of surgery. An infusion of 0.01% phenylephrine was used as necessary to maintain mean arterial pressure at baseline levels. Results Although both agents increased blood flow velocity in the middle cerebral artery at 0.5 and 1.5 MAC, this increase was significantly less during sevoflurane anesthesia (4+/-3 and 17+/-3% at 0.5 and 1.5 MAC sevoflurane; 19+/-3 and 72+/-9% at 0.5 and 1.5 MAC isoflurane [mean +/- SD]; P&lt;0.05). All patients required phenylephrine (100-300 microg) to maintain mean arterial pressure within 20% of baseline during 1.5 MAC anesthesia. Conclusions In common with other volatile anesthetic agents, sevoflurane has an intrinsic dose-dependent cerebral vasodilatory effect. However, this effect is less than that of isoflurane.

Cerebral Blood Flow in Acute Mountain Sickness and Treatment with Acetazolamide

1988 ◽  
Vol 74 (s18) ◽  
pp. 1P-1P ◽  
Author(s):  
AD Wright ◽  
AR Bradwell ◽  
J Jensen ◽  
N Lassen
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Acute Mountain Sickness ◽  
Mountain Sickness

scholarly journals Sustained high-altitude hypoxia increases cerebral oxygen metabolism

2013 ◽  
Vol 114 (1) ◽  
pp. 11-18 ◽  
Author(s):  
Zachary M. Smith ◽  
Erin Krizay ◽  
Jia Guo ◽  
David D. Shin ◽  
Miriam Scadeng ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
High Altitude ◽  
Acute Mountain Sickness ◽  
Oxygen Metabolism ◽  
Cerebral Oxygen ◽  
Altitude Hypoxia ◽  
Cerebral Oxygen Metabolism ◽  
High Altitude Hypoxia ◽  
Significant Difference

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.

Slow oscillations in middle cerebral artery cerebral blood flow velocity and aging

2007 ◽  
Vol 29 (3) ◽  
pp. 260-263 ◽  
Author(s):  
Philip M. Lewis ◽  
Piotr Smielewski ◽  
John D. Pickard ◽  
Marek Czosnyka
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Middle Cerebral Artery ◽  
Flow Velocity ◽  
Cerebral Artery ◽  
Blood Flow Velocity ◽  
Cerebral Blood Flow Velocity ◽  
Slow Oscillations

scholarly journals Regional cerebral blood flow during acute hypoxia in individuals susceptible to acute mountain sickness

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
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Regional Cerebral Blood Flow ◽  
Acute Hypoxia ◽  
Acute Mountain Sickness ◽  
Regional Cerebral Blood ◽  
Mountain Sickness

New insights into ocular blood flow at very high altitudes

2009 ◽  
Vol 106 (2) ◽  
pp. 454-460 ◽  
Author(s):  
Martina M. Bosch ◽  
Tobias M. Merz ◽  
Daniel Barthelmes ◽  
Benno L. Petrig ◽  
Frederic Truffer ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
High Altitude ◽  
Cerebral Edema ◽  
Arterial Oxygen Saturation ◽  
Acute Mountain Sickness ◽  
Fundus Photography ◽  
Arterial Oxygen ◽  
High Altitudes ◽  
Choroidal Blood Flow

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.

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