CT scan imaging of cerebral oxygen metabolism indices and blood flow

2003 ◽  
Author(s):  
H. Ono ◽  
H. Ishizaka ◽  
A.H. Rowberg
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.


2012 ◽  
Vol 323 (1-2) ◽  
pp. 173-177 ◽  
Author(s):  
Zhaoxia Wang ◽  
Jiangxi Xiao ◽  
Sheng Xie ◽  
Danhua Zhao ◽  
Xiwei Liu ◽  
...  

1990 ◽  
Vol 28 (1) ◽  
pp. 50-51 ◽  
Author(s):  
Billie Lou Short ◽  
L Kyle Walker ◽  
Christine A Gleason ◽  
M Douglas Jones ◽  
Richard J Traystman

1991 ◽  
Vol 557 (1-2) ◽  
pp. 217-220 ◽  
Author(s):  
Peter Lund Madsen ◽  
Jes F. Schmidt ◽  
Søren Holm ◽  
Sissel Vorstrup ◽  
Niels A. Lassen ◽  
...  

1987 ◽  
Vol 27 (3) ◽  
pp. 155-163 ◽  
Author(s):  
Yoshiyasu Tsuda ◽  
Kazufumi Kimura ◽  
Shotaro Yoneda ◽  
Alexander Hartmann ◽  
Hideki Etani ◽  
...  

2021 ◽  
Author(s):  
Michael Germuska ◽  
Rachael C Stickland ◽  
Antonio Maria Chiarelli ◽  
Hannah L Chandler ◽  
Richard G Wise

Magnetic resonance imaging (MRI) offers the possibility to non-invasively map the rate of cerebral metabolic oxygen consumption (CMRO2), which is essential for understanding and monitoring neural function in both health and disease. Existing methods of mapping CMRO2, based on respiratory modulation of arterial spin labelling (ASL) and blood oxygen level dependent (BOLD) signals, require lengthy acquisitions and independent modulation of both arterial oxygen and carbon dioxide levels. Here, we present a new simplified method for mapping the rate of cerebral oxygen metabolism that can be performed using a simple breath-holding paradigm. The method incorporates flow-diffusion modelling of oxygen transport and physiological constraints to create a non-linear mapping between the maximum BOLD signal, M, baseline blood flow (CBF0), and CMRO2. A gradient boosted decision tree is used to learn this mapping directly from simulated MRI data. Modelling studies demonstrate that the proposed method is robust to variation in cerebral physiology and metabolism. This new gas-free methodology offers a rapid and pragmatic alternative to existing dual-calibrated methods, removing the need for specialist respiratory equipment and long acquisition times. In-vivo testing of the method, using an 8-minute 45 second protocol of repeated breath-holding, was performed on 15 healthy volunteers, producing quantitative maps of cerebral blood flow (CBF), oxygen extraction fraction (OEF), and CMRO2.


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