scholarly journals The middle cerebral artery blood velocity response to acute normobaric hypoxia occurs independently of changes in ventilation in humans

2021 ◽  
Author(s):  
Sultan E. AlSalahi ◽  
Rehan T. Junejo ◽  
Chris Bradley ◽  
George M. Balanos ◽  
Christoph Siebenmann ◽  
...  
2012 ◽  
Vol 26 (S1) ◽  
Author(s):  
Elisa Wasson ◽  
Cody Harper ◽  
Andrew Subudhi ◽  
Sue Schneider ◽  
Nico Maestas ◽  
...  

VASA ◽  
1999 ◽  
Vol 28 (4) ◽  
pp. 279-282 ◽  
Author(s):  
Müller ◽  
Behnke ◽  
Walter

Background: To study the pattern of cerebral blood flow velocity and cerebral resistance changes after carotid endarterectomy. Patients and methods: In 81 patients (mean age ± SD, 64 ± 8 years) with unilateral carotid endarterectomy (CEA) the systolic, diastolic and mean blood velocities, and the pulsatility index (PI) were recorded in both middle cerebral arteries preoperatively and repetitively postoperatively with the use of transcranial Doppler ultrasound (TCD). Results: In the middle cerebral artery ipsilateral to CEA mean blood velocity was increased 6 hours (64 ± 25 cm/sec; p < 0.005) and 7 days (54 ± 15 cm/sec; p < 0.05) after CEA and had returned to the preoperative level (49 ± 11 cm/sec) after 3 months. Compared to preoperatively (0.86 ±. 22), the PI was significantly increased at 6 hours examination (1.03 ±. 23, p < 0.005), and remained increased thereafter. A pathologically increased mean blood velocity (> 83 cm/sec) 6 hours after CEA occurred in 11 patients, two of them developed a slight hyperperfusion syndrome. In the contralateral middle cerebral artery, only the diastolic blood velocity showed significant changes (preoperatively, 35 ± 12 cm/sec; 3 months after CEA, 33 ± 8 cm/sec; p < 0.05). Conclusions: Using TCD, hemodynamic changes occur predominantly in the middle cerebral arteries ipsilateral to CEA. Early postoperative TCD studies may be of help to identify patients at risk to develop a hyperperfusion syndrome.


Author(s):  
Alykhan Kurji ◽  
Chantel T. Debert ◽  
William A. Whitelaw ◽  
Jean M. Rawling ◽  
Richard Frayne ◽  
...  

Author(s):  
Mohammed R. Alwatban ◽  
Stacey E. Aaron ◽  
Carolyn S. Kaufman ◽  
Jill N. Barnes ◽  
Patrice Brassard ◽  
...  

Reduced middle cerebral artery blood velocity (MCAv) and flow pulsatility are contributors to age-related cerebrovascular disease pathogenesis. It is unknown whether the rate of changes in MCAv and flow pulsatility support the hypothesis of sex specific trajectories with aging. Therefore, we sought to characterize the rate of changes in MCAv and flow pulsatility across the adult lifespan in females and males as well as within specified age ranges. Participant characteristics, mean arterial pressure, end-tidal carbon dioxide, unilateral MCAv and flow pulsatility index (PI) were determined from study records compiled from three institutional sites. 524 participants (18-90 years; 319 females; 205 males) were included in the analysis. MCAv was significantly higher in females within the 2nd (p <0.001), 5th (p = 0.01), and 6th (p <0.01) decades of life. Flow PI was significantly higher in females within the 2nd decade of life (p <0.01). Rate of MCAv decline was significantly greater in females than males (-0.39 vs. -0.26 cm s-1·yr, p = 0.04). Rate of flow PI rise was significantly greater in females than males (0.006 vs. 0.003 flow PI, p = 0.01). Rate of MCAv change was significantly greater in females than males in the 6th decade of life (-1.44 vs. 0.13 cm s-1·yr), p = 0.04). These findings indicate that sex significantly contributes to age-related differences in both MCAv and flow PI. Therefore, further investigation into cerebrovascular function within and between sexes is warranted to improve our understanding of the reported sex differences in cerebrovascular disease prevalence.


2013 ◽  
Vol 114 (1) ◽  
pp. 37-44 ◽  
Author(s):  
Joshua F. Lee ◽  
Michelle L. Harrison ◽  
Skyler R. Brown ◽  
R. Matthew Brothers

The mechanisms responsible for heat stress-induced reductions in tolerance to a simulated hemorrhage are unclear. Although a high degree of variability exists in the level of reduction in tolerance amongst individuals, syncope will always occur when cerebral perfusion is inadequate. This study tested the hypothesis that the magnitude of reduction in cerebral perfusion during heat stress is related to the reduction in tolerance to a lower body negative pressure (LBNP) challenge. On different days (one during normothermia and the other after a 1.5°C rise in internal temperature), 20 individuals were exposed to a LBNP challenge to presyncope. Tolerance was quantified as a cumulative stress index, and the difference in cumulative stress index between thermal conditions was used to categorize individuals most (large difference) and least (small difference) affected by the heat stress. Cerebral perfusion, as indexed by middle cerebral artery blood velocity, was reduced during heat stress compared with normothermia ( P < 0.001); however, the magnitude of reduction did not differ between groups ( P = 0.51). In the initial stage of LBNP during heat stress (LBNP 20 mmHg), middle cerebral artery blood velocity and end-tidal Pco2 were lower; whereas, heart rate was higher in the large difference group compared with small difference group ( P < 0.05 for all). These data indicate that variability in heat stress-induced reductions in tolerance to a simulated hemorrhage is not related to reductions in cerebral perfusion in this thermal condition. However, responses affecting cerebral perfusion during LBNP may explain the interindividual variability in tolerance to a simulated hemorrhage when heat stressed.


2007 ◽  
Vol 106 (1) ◽  
pp. 56-64 ◽  
Author(s):  
Timothy J. McCulloch ◽  
Christopher L. Thompson ◽  
Martin J. Turner

Background Intravenous and inhalational anesthetic agents have differing effects on cerebral hemodynamics: Sevoflurane causes some vasodilation, whereas propofol does not. The authors hypothesized that these differences affect internal carotid artery pressure (ICAP) and the apparent zero flow pressure (critical closing pressure) during carotid endarterectomy. Vasodilation is expected to increase blood flow, reduce ICAP, and reduce apparent zero flow pressure. Methods In a randomized crossover study, the gradient between systemic arterial pressure and ICAP during carotid clamping was measured while changing between sevoflurane and propofol in 32 patients. Middle cerebral artery blood velocity, recorded by transcranial Doppler, and ICAP waveforms were analyzed to determine the apparent zero flow pressure. Results ICAP increased when changing from sevoflurane to propofol, causing the mean gradient between arterial pressure and ICAP to decrease by 10 mmHg (95% confidence interval, 6-14 mmHg; P&lt;0.0001). Changing from propofol to sevoflurane had the opposite effect: The pressure gradient increased by 5 mmHg (95% confidence interval, 2-7 mmHg; P=0.002). Ipsilateral middle cerebral artery blood velocity decreased when changing from sevoflurane to propofol. Cerebral steal was detected in one patient after changing from propofol to sevoflurane. The apparent zero flow pressure (mean+/-SD) was 22+/-10 mmHg with sevoflurane and 30+/-14 mmHg with propofol (P&lt;0.01). There was incomplete drug crossover due to the limited duration of carotid clamping. Conclusions Compared with sevoflurane, ipsilateral ICAP and apparent zero flow pressure are both higher with propofol. Vasodilatation associated with sevoflurane can cause cerebral steal.


Stroke ◽  
1991 ◽  
Vol 22 (12) ◽  
pp. 1508-1511 ◽  
Author(s):  
A Postiglione ◽  
F Faccenda ◽  
G Gallotta ◽  
P Rubba ◽  
S Federico

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