Internal carotid and vertebral arterial flow velocity in men at high altitude

1987 ◽  
Vol 63 (1) ◽  
pp. 395-400 ◽  
Author(s):  
S. Y. Huang ◽  
L. G. Moore ◽  
R. E. McCullough ◽  
R. G. McCullough ◽  
A. J. Micco ◽  
...  

Cerebral blood flow increases at high altitude, but the mechanism of the increase and its role in adaptation to high altitude are unclear. We hypothesized that the hypoxemia at high altitude would increase cerebral blood flow, which would in turn defend O2 delivery to the brain. Noninvasive Doppler ultrasound was used to measure the flow velocities in the internal carotid and the vertebral arteries in six healthy male subjects. Within 2–4 h of arrival on Pikes Peak (4,300 m), velocities in both arteries were slightly and not significantly increased above sea-level values. By 18–44 h a peak increase of 20% was observed (combined P less than 0.025). Subsequently (days 4–12) velocities declined to values similar to those at sea level. At altitude the lowest arterial O2 saturation (SaO2) and the highest end-tidal PCO2 was observed on arrival. By day 4 and thereafter, when the flow velocities had returned toward sea-level values, hemoglobin concentration and SaO2 were increased over initial high-altitude values such that calculated O2 transport values were even higher than those at sea level. Although the cause of the failure for cerebral flow velocity to increase on arrival is not understood, the subsequent increase may act to defend brain O2 transport. With further increase in hemoglobin and SaO2 over time at high altitude, flow velocity returned to sea-level values.

2011 ◽  
Vol 91 (10) ◽  
pp. 1503-1512 ◽  
Author(s):  
Abigail Jade Hunter ◽  
Suzanne J. Snodgrass ◽  
Debbie Quain ◽  
Mark W. Parsons ◽  
Christopher R. Levi

BackgroundCerebral autoregulation can be impaired after ischemic stroke, with potential adverse effects on cerebral blood flow during early rehabilitation.ObjectiveThe objective of this study was to assess changes in cerebral blood flow velocity with orthostatic variation at 24 hours after stroke.DesignThis investigation was an observational study comparing mean flow velocities (MFVs) at 30, 15, and 0 degrees of elevation of the head of the bed (HOB).MethodsEight participants underwent bilateral middle cerebral artery (MCA) transcranial Doppler monitoring during orthostatic variation at 24 hours after ischemic stroke. Computed tomography angiography separated participants into recanalized (artery completely reopened) and incompletely recanalized groups. Friedman tests were used to determine MFVs at the various HOB angles. Mann-Whitney U tests were used to compare the change in MFV (from 30° to 0°) between groups and between hemispheres within groups.ResultsFor stroke-affected MCAs in the incompletely recanalized group, MFVs differed at the various HOB angles (30°: median MFV=51.5 cm/s, interquartile range [IQR]=33.0 to 103.8; 15°: median MFV=55.5 cm/s, IQR=34.0 to 117.5; 0°: median MFV=85.0 cm/s, IQR=58.8 to 127.0); there were no significant differences for other MCAs. For stroke-affected MCAs in the incompletely recanalized group, MFVs increased with a change in the HOB angle from 30 degrees to 0 degrees by a median of 26.0 cm/s (IQR=21.3 to 35.3); there were no significant changes in the recanalized group (−3.5 cm/s, IQR=−12.3 to 0.8). The changes in MFV with a change in the HOB angle from 30 degrees to 0 degrees differed between hemispheres in the incompletely recanalized group but not in the recanalized group.LimitationsGeneralizability was limited by sample size.ConclusionsThe incompletely recanalized group showed changes in MFVs at various HOB angles, suggesting that cerebral blood flow in this group may be sensitive to orthostatic variation, whereas the recanalized group maintained stable blood flow velocities.


2017 ◽  
Vol 122 (4) ◽  
pp. 795-808 ◽  
Author(s):  
Ryan L. Hoiland ◽  
Anthony R. Bain ◽  
Michael M. Tymko ◽  
Mathew G. Rieger ◽  
Connor A. Howe ◽  
...  

Hypoxia increases cerebral blood flow (CBF) with the underlying signaling processes potentially including adenosine. A randomized, double-blinded, and placebo-controlled design, was implemented to determine if adenosine receptor antagonism (theophylline, 3.75 mg/Kg) would reduce the CBF response to normobaric and hypobaric hypoxia. In 12 participants the partial pressures of end-tidal oxygen ([Formula: see text]) and carbon dioxide ([Formula: see text]), ventilation (pneumotachography), blood pressure (finger photoplethysmography), heart rate (electrocardiogram), CBF (duplex ultrasound), and intracranial blood velocities (transcranial Doppler ultrasound) were measured during 5-min stages of isocapnic hypoxia at sea level (98, 90, 80, and 70% [Formula: see text]). Ventilation, [Formula: see text] and [Formula: see text], blood pressure, heart rate, and CBF were also measured upon exposure (128 ± 31 min following arrival) to high altitude (3,800 m) and 6 h following theophylline administration. At sea level, although the CBF response to hypoxia was unaltered pre- and postplacebo, it was reduced following theophylline ( P < 0.01), a finding explained by a lower [Formula: see text] ( P < 0.01). Upon mathematical correction for [Formula: see text], the CBF response to hypoxia was unaltered following theophylline. Cerebrovascular reactivity to hypoxia (i.e., response slope) was not different between trials, irrespective of [Formula: see text]. At high altitude, theophylline ( n = 6) had no effect on CBF compared with placebo ( n = 6) when end-tidal gases were comparable ( P > 0.05). We conclude that adenosine receptor-dependent signaling is not obligatory for cerebral hypoxic vasodilation in humans. NEW & NOTEWORTHY The signaling pathways that regulate human cerebral blood flow in hypoxia remain poorly understood. Using a randomized, double-blinded, and placebo-controlled study design, we determined that adenosine receptor-dependent signaling is not obligatory for the regulation of human cerebral blood flow at sea level; these findings also extend to high altitude.


2017 ◽  
Vol 123 (4) ◽  
pp. 1003-1010 ◽  
Author(s):  
Daniela Flück ◽  
Laura E. Morris ◽  
Shailesh Niroula ◽  
Christine M. Tallon ◽  
Kami T. Sherpa ◽  
...  

Developmental cerebral hemodynamic adaptations to chronic high-altitude exposure, such as in the Sherpa population, are largely unknown. To examine hemodynamic adaptations in the developing human brain, we assessed common carotid (CCA), internal carotid (ICA), and vertebral artery (VA) flow and middle cerebral artery (MCA) velocity in 25 (9.6 ± 1.0 yr old, 129 ± 9 cm, 27 ± 8 kg, 14 girls) Sherpa children (3,800 m, Nepal) and 25 (9.9 ± 0.7 yr old, 143 ± 7 cm, 34 ± 6 kg, 14 girls) age-matched sea level children (344 m, Canada) during supine rest. Resting gas exchange, blood pressure, oxygen saturation and heart rate were assessed. Despite comparable age, height and weight were lower (both P < 0.01) in Sherpa compared with sea level children. Mean arterial pressure, heart rate, and ventilation were similar, whereas oxygen saturation (95 ± 2 vs. 99 ± 1%, P < 0.01) and end-tidal Pco2 (24 ± 3 vs. 36 ± 3 Torr, P < 0.01) were lower in Sherpa children. Global cerebral blood flow was ∼30% lower in Sherpa compared with sea level children. This was reflected in a lower ICA flow (283 ± 108 vs. 333 ± 56 ml/min, P = 0.05), VA flow (78 ± 26 vs. 118 ± 35 ml/min, P < 0.05), and MCA velocity (72 ± 14 vs. 88 ± 14 cm/s, P < 0.01). CCA flow was similar between Sherpa and sea level children (425 ± 92 vs. 441 ± 81 ml/min, P = 0.52). Scaling flow and oxygen uptake for differences in vessel diameter and body size, respectively, led to the same findings. A lower cerebral blood flow in Sherpa children may reflect specific cerebral hemodynamic adaptations to chronic hypoxia. NEW & NOTEWORTHY Cerebral blood flow is lower in Sherpa children compared with children residing at sea level; this may reflect a cerebral hemodynamic pattern, potentially due to adaptation to a hypoxic environment.


1985 ◽  
Vol 59 (3) ◽  
pp. 909-915 ◽  
Author(s):  
J. T. Reeves ◽  
L. G. Moore ◽  
R. E. McCullough ◽  
R. G. McCullough ◽  
G. Harrison ◽  
...  

The cause of headache in persons going to high altitude is unknown. Relatively severe hypoxemia in susceptible subjects could induce large increases in cerebral blood flow that then could initiate the headache. Thus we measured noninvasively, by Doppler ultrasound, changes in internal carotid arterial blood velocity (velocity) in 12 subjects in Denver (1,600 m) and repeatedly up to 7 h at a simulated altitude of 4,800 m (barometric pressure = 430 Torr). Six subjects, selected because of prior history of high-altitude headache, developed comparatively severe headache at 4,800 m, and four subjects, without such history, remained well. Two subjects developed moderate headache. Velocity at 4,800 m did not correlate with symptom development, arterial O2 saturation, or end-tidal PCO2. Also, neither velocity nor blood pressure was consistently elevated above the Denver base-line values. During measurements of hypercapnic ventilatory response in Denver, velocity increased linearly with end-tidal PCO2, confirming that our Doppler method could demonstrate an increase. Also, 30 min of isocapnic or poikilocapnic hypoxia caused small increases in velocity (+8 and +6%) during the base-line measurement at low altitude. Although even a small increase in cerebral perfusion could contribute to headache symptoms at high altitude, cerebral blood flow does not appear to play a primary role.


2014 ◽  
Vol 116 (7) ◽  
pp. 905-910 ◽  
Author(s):  
C. K. Willie ◽  
K. J. Smith ◽  
T. A. Day ◽  
L. A. Ray ◽  
N. C. S. Lewis ◽  
...  

The interindividual variation in ventilatory acclimatization to high altitude is likely reflected in variability in the cerebrovascular responses to high altitude, particularly between brain regions displaying disparate hypoxic sensitivity. We assessed regional differences in cerebral blood flow (CBF) measured with Duplex ultrasound of the left internal carotid and vertebral arteries. End-tidal Pco2, oxyhemoglobin saturation (SpO2), blood pressure, and heart rate were measured during a trekking ascent to, and during the first 2 wk at, 5,050 m. Transcranial color-coded Duplex ultrasound (TCCD) was employed to measure flow and diameter of the middle cerebral artery (MCA). Measures were collected at 344 m (TCCD-baseline), 1,338 m (CBF-baseline), 3,440 m, and 4,371 m. Following arrival to 5,050 m, regional CBF was measured every 12 h during the first 3 days, once at 5–9 days, and once at 12–16 days. Total CBF was calculated as twice the sum of internal carotid and vertebral flow and increased steadily with ascent, reaching a maximum of 842 ± 110 ml/min (+53 ± 7.6% vs. 1,338 m; mean ± SE) at ∼60 h after arrival at 5,050 m. These changes returned to +15 ± 12% after 12–16 days at 5,050 m and were related to changes in SpO2 ( R2 = 0.36; P < 0.0001). TCCD-measured MCA flow paralleled the temporal changes in total CBF. Dilation of the MCA was sustained on days 2 (+12.6 ± 4.6%) and 8 (+12.9 ± 2.9%) after arrival at 5,050 m. We observed no significant differences in regional CBF at any time point. In conclusion, the variability in CBF during ascent and acclimatization is related to ventilatory acclimatization, as reflected in changes in SpO2.


2011 ◽  
Vol 165 (3) ◽  
pp. 465-468 ◽  
Author(s):  
Uygar Utku ◽  
Mustafa Gokce ◽  
Mesut Özkaya

BackgroundAt present, hypothyroidism is a well-known risk factor for cardiovascular disorders. The aim of this study was to assess the effects of hypothyroidism on cerebral blood flow velocity with transcranial Doppler (TCD) ultrasonography.Design and methodsIn this study, 30 subjects were enrolled for clinical, subclinical, and healthy control groups. Bilateral middle cerebral artery (MCA) peak-systolic, end-diastolic, and mean blood flow velocities; Gosling's pulsatility index values; and Pourcelot's resistance index values were recorded and compared with each other. TCD was performed in clinical hypothyroid patients after they became euthyroid with thyroid hormone replacement therapy (HRT). The initial and post-HRT results for the clinical hypothyroid group were then compared and evaluated.ResultsThere were 30 subjects in each group. Men/women ratio and mean age in clinical hypothyroid, subclinical hypothyroid, and control groups were 3/27, 4/26, and 5/25, and 37.4, 34.4, and 36.7 respectively. Peak-systolic, end-diastolic, and mean blood flow velocities of bilateral MCA were similar in clinical and subclinical hypothyroid groups but significantly higher when compared with the control group. After adequate thyroid HRT in clinical hypothyroid group, the peak-systolic, end-diastolic, and mean blood flow velocities were significantly decreased.ConclusionsIncreased cerebral blood flow velocities were observed in clinical and subclinical patients with hypothyroidism. The normalization of increased blood flow velocity with thyroid HRT suggests a reversible condition.


2010 ◽  
Vol 41 (01) ◽  
Author(s):  
B Feddersen ◽  
H Ausserer ◽  
R Waanders ◽  
S Noachtar ◽  
T Pfefferkorn

2002 ◽  
Vol 22 (1) ◽  
pp. 118-126 ◽  
Author(s):  
Kirsten Møller ◽  
Olaf B. Paulson ◽  
Tom F. Hornbein ◽  
Wil N. J. M. Colier ◽  
Anna S. Paulson ◽  
...  

The authors investigated the effect of acclimatization to high altitude on cerebral blood flow and oxidative metabolism at rest and during exercise. Nine healthy, native sea-level residents were studied 3 weeks after arrival at Chacaltaya, Bolivia (5,260 m) and after reacclimatization to sea level. Global cerebral blood flow at rest and during exercise on a bicycle ergometer was measured by the Kety-Schmidt technique. Cerebral metabolic rates of oxygen, glucose, and lactate were calculated by the Fick principle. Cerebral function was assessed by a computer-based measurement of reaction time. At high altitude at rest, arterial carbon dioxide tension, oxygen saturation, and oxygen tension were significantly reduced, and arterial oxygen content was increased because of an increase in hemoglobin concentration. Global cerebral blood flow was similar in the four conditions. Cerebral oxygen delivery and cerebral metabolic rates of oxygen and glucose also remained unchanged, whereas cerebral metabolic rates of lactate increased slightly but nonsignificantly at high altitude during exercise compared with high altitude at rest. Reaction time was unchanged. The data indicate that cerebral blood flow and oxidative metabolism are unaltered after high-altitude acclimatization from sea level, despite marked changes in breathing and other organ functions.


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