Breath holding test in preeclampsia: lack of evidence for altered cerebral vascular reactivity

2002 ◽  
Vol 11 (3) ◽  
pp. 160-163 ◽  
Author(s):  
J. Zatik ◽  
J. Aranyosi ◽  
G. Settakis ◽  
D. PÁll ◽  
Z. Tóth ◽  
...  
Keyword(s):  
Vascular Reactivity ◽  
Breath Holding ◽  
Cerebral Vascular

scholarly journals Comparison of Cerebral Vascular Reactivity Measures Obtained Using Breath-Holding and CO2 Inhalation

2013 ◽  
Vol 33 (7) ◽  
pp. 1066-1074 ◽  
Author(s):  
Felipe B Tancredi ◽  
Richard D Hoge
Keyword(s):  
Arterial Spin Labeling ◽  
Vascular Reactivity ◽  
Automated System ◽  
Breath Holding ◽  
Breath Hold ◽  
Cerebral Vasculature ◽  
Fixed Concentration ◽  
Physiologic Modeling ◽  
End Tidal ◽  
Cerebral Vascular

Stimulation of cerebral vasculature using hypercapnia has been widely used to study cerebral vascular reactivity (CVR), which can be expressed as the quantitative change in cerebral blood flow (CBF) per mm Hg change in end-tidal partial pressure of CO2 (PETCO2). We investigate whether different respiratory manipulations, with arterial spin labeling used to measure CBF, lead to consistent measures of CVR. The approaches included: (1) an automated system delivering variable concentrations of inspired CO2 for prospective targeting of PETCO2, (2) administration of a fixed concentration of CO2 leading to subject-dependent changes in PETCO2, (3) a breath-hold (BH) paradigm with physiologic modeling of CO2 accumulation, and (4) a maneuver combining breath-hold and hyperventilation. When CVR was expressed as the percent change in CBF per mm Hg change in PETCO2, methods 1 to 3 gave consistent results. The CVR values using method 4 were significantly lower. When CVR was expressed in terms of the absolute change in CBF (mL/100g per minute per mm Hg), greater discrepancies became apparent: methods 2 and 3 gave lower absolute CVR values compared with method 1, and the value obtained with method 4 was dramatically lower. Our findings indicate that care must be taken to ensure that CVR is measured over the linear range of the CBF-CO2 dose-response curve, avoiding hypocapnic conditions.

scholarly journals The Adverse Pial Arteriolar and Axonal Consequences of Traumatic Brain Injury Complicated by Hypoxia and Their Therapeutic Modulation with Hypothermia in Rat

2009 ◽  
Vol 30 (3) ◽  
pp. 628-637 ◽  
Author(s):  
Guoyi Gao ◽  
Yasutaka Oda ◽  
Enoch P Wei ◽  
John T Povlishock
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Amyloid Precursor Protein ◽  
Vascular Reactivity ◽  
Axonal Damage ◽  
Precursor Protein ◽  
Moderate Hypothermia ◽  
Vascular Protection ◽  
Impact Acceleration ◽  
Cerebral Vascular

This study examined the effect of posttraumatic hypoxia on cerebral vascular responsivity and axonal damage, while also exploring hypothermia's potential to attenuate these responses. Rats were subjected to impact acceleration injury (IAI) and equipped with cranial windows to assess vascular reactivity to topical acetylcholine, with postmortem analyses using antibodies to amyloid precursor protein to assess axonal damage. Animals were subjected to hypoxia alone, IAI and hypoxia, IAI and hypoxia before induction of moderate hypothermia (33°C), IAI and hypoxia induced during hypothermic intervention, and IAI and hypoxia initiated after hypothermia. Hypoxia alone had no impact on vascular reactivity or axonal damage. Acceleration injury and posttraumatic hypoxia resulted in dramatic axonal damage and altered vascular reactivity. When IAI and hypoxia were followed by hypothermic intervention, no axonal or vascular protection ensued. However, when IAI was followed by hypoxia induced during hypothermia, axonal and vascular protection followed. When this same hypoxic insult followed the use of hypothermia, no benefit ensued. These studies show that early hypoxia and delayed hypoxia exert damaging axonal and vascular consequences. Although this damage is attenuated by hypothermia, this follows only when hypoxia occurs during hypothermia, with no benefit found if the hypoxic insult proceeds or follows hypothermia.

scholarly journals Preservation of Cerebral Vascular Reactivity by Sodium Channel Inhibition in Acute Prolonged Asphyxic Brain Injury (ABI) in Piglets

1999 ◽  
Vol 45 (6) ◽  
pp. 910-910
Author(s):  
Vladimir Levine ◽  
Massroor Pourcyrous ◽  
Henrietta Bada ◽  
Wenjian Yang ◽  
Sheldon Korones ◽  
...  
Keyword(s):  
Brain Injury ◽  
Sodium Channel ◽  
Vascular Reactivity ◽  
Channel Inhibition ◽  
Cerebral Vascular

scholarly journals Relationship Between 25(OH) Vitamin D3 and Cerebral Vascular Reactivity in College-aged African and Caucasian Americans

2014 ◽  
Vol 46 ◽  
pp. 749
Author(s):  
Chansol Hurr ◽  
Kiyoung Kim ◽  
Michelle L. Harrison ◽  
Joshua F. Lee ◽  
Kevin M. Christmas ◽  
...  
Keyword(s):  
Vitamin D3 ◽  
Vascular Reactivity ◽  
Caucasian Americans ◽  
Cerebral Vascular

Whole-brain vascular reactivity measured by fMRI using hyperventilation and breath-holding tasks: efficacy of 3D prospective acquisition correction (3D-PACE) for head motion

2004 ◽  
Vol 14 (8) ◽  
Author(s):  
Shinji Naganawa ◽  
Tokiko Koshikawa ◽  
Hiroshi Fukatsu ◽  
Takeo Ishigaki ◽  
Katsuya Maruyama ◽  
...  
Keyword(s):  
Vascular Reactivity ◽  
Breath Holding ◽  
Head Motion ◽  
Whole Brain

scholarly journals Vascular Reactivity Maps in Patients with Gliomas Using Breath-Holding BOLD fMRI

2015 ◽  
Vol 26 (2) ◽  
pp. 232-239 ◽  
Author(s):  
Amir Iranmahboob ◽  
Kyung K. Peck ◽  
Nicole P. Brennan ◽  
Sasan Karimi ◽  
Ryan Fisicaro ◽  
...  
Keyword(s):  
Vascular Reactivity ◽  
Breath Holding ◽  
Bold Fmri

Acute effects of tibolone on cerebral vascular reactivity in vitro

Climacteric ◽  
2003 ◽  
Vol 6 (3) ◽  
pp. 228-237 ◽  
Author(s):  
C. O. Lund ◽  
L. Nilas ◽  
T. Dalsgaard ◽  
S. H. Pedersen ◽  
B. Ottesen
Keyword(s):  
Vascular Reactivity ◽  
Acute Effects ◽  
Cerebral Vascular

Hypercapnic cerebral vascular reactivity is decreased, in humans, during sleep compared with wakefulness

2003 ◽  
Vol 94 (6) ◽  
pp. 2197-2202 ◽  
Author(s):  
Guy E. Meadows ◽  
Helen M. A. Dunroy ◽  
Mary J. Morrell ◽  
Douglas R. Corfield
Keyword(s):  
Blood Flow ◽  
Vascular Reactivity ◽  
Nrem Sleep ◽  
Normal Subjects ◽  
Stage Iii ◽  
Left Middle Cerebral Artery ◽  
Cortical Blood Flow ◽  
Pulsed Doppler Ultrasound ◽  
End Tidal ◽  
Cerebral Vascular

During wakefulness, increases in the partial pressure of arterial CO2 result in marked rises in cortical blood flow. However, during stage III–IV, non-rapid eye movement (NREM) sleep, and despite a relative state of hypercapnia, cortical blood flow is reduced compared with wakefulness. In the present study, we tested the hypothesis that, in normal subjects, hypercapnic cerebral vascular reactivity is decreased during stage III–IV NREM sleep compared with wakefulness. A 2-MHz pulsed Doppler ultrasound system was used to measure the left middle cerebral artery velocity (MCAV; cm/s) in 12 healthy individuals while awake and during stage III–IV NREM sleep. The end-tidal Pco 2(Pet CO2 ) was elevated during the awake and sleep states by regulating the inspired CO2 load. The cerebral vascular reactivity to CO2 was calculated from the relationship between Pet CO2 and MCAV by using linear regression. From wakefulness to sleep, the Pet CO2 increased by 3.4 Torr ( P < 0.001) and the MCAV fell by 11.7% ( P < 0.001). A marked decrease in cerebral vascular reactivity was noted in all subjects, with an average fall of 70.1% ( P = 0.001). This decrease in hypercapnic cerebral vascular reactivity may, at least in part, explain the stage III–IV NREM sleep-related reduction in cortical blood flow.

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