Assessment of middle cerebral artery diameter during hypocapnia and hypercapnia in humans using ultra-high-field MRI
In the evaluation of cerebrovascular CO 2 reactivity measurements, it is often assumed that the diameter of the large intracranial arteries insonated by transcranial Doppler remains unaffected by changes in arterial CO 2 partial pressure. However, the strong cerebral vasodilatory capacity of CO 2 ch...
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| Published in | Journal of applied physiology (1985) Vol. 117; no. 10; pp. 1084 - 1089 |
|---|---|
| Main Authors | , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
United States
American Physiological Society
15.11.2014
|
| Subjects | |
| Online Access | Get full text |
| ISSN | 8750-7587 1522-1601 1522-1601 |
| DOI | 10.1152/japplphysiol.00651.2014 |
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| Abstract | In the evaluation of cerebrovascular CO
2
reactivity measurements, it is often assumed that the diameter of the large intracranial arteries insonated by transcranial Doppler remains unaffected by changes in arterial CO
2
partial pressure. However, the strong cerebral vasodilatory capacity of CO
2
challenges this assumption, suggesting that there should be some changes in diameter, even if very small. Data from previous studies on effects of CO
2
on cerebral artery diameter [middle cerebral artery (MCA)] have been inconsistent. In this study, we examined 10 healthy subjects (5 women, 5 men, age 21–30 yr). High-resolution (0.2 mm in-plane) MRI scans at 7 Tesla were used for direct observation of the MCA diameter during hypocapnia, −1 kPa (−7.5 mmHg), normocapnia, 0 kPa (0 mmHg), and two levels of hypercapnia, +1 and +2 kPa (7.5 and 15 mmHg), with respect to baseline. The vessel lumen was manually delineated by two independent observers. The results showed that the MCA diameter increased by 6.8 ± 2.9% in response to 2 kPa end-tidal Pco
2
(Pet
CO
2
) above baseline. However, no significant changes in diameter were observed at the −1 kPa (−1.2 ± 2.4%), and +1 kPa (+1.4 ± 3.2%) levels relative to normocapnia. The nonlinear response of the MCA diameter to CO
2
was fitted as a continuous calibration curve. Cerebral blood flow changes measured by transcranial Doppler could be corrected by this calibration curve using concomitant Pet
CO
2
measurements. In conclusion, the MCA diameter remains constant during small deviations of the Pet
CO
2
from normocapnia, but increases at higher Pet
CO
2
values. |
|---|---|
| AbstractList | In the evaluation of cerebrovascular CO2 reactivity measurements, it is often assumed that the diameter of the large intracranial arteries insonated by transcranial Doppler remains unaffected by changes in arterial CO2 partial pressure. However, the strong cerebral vasodilatory capacity of CO2 challenges this assumption, suggesting that there should be some changes in diameter, even if very small. Data from previous studies on effects of CO2 on cerebral artery diameter [middle cerebral artery (MCA)] have been inconsistent. In this study, we examined 10 healthy subjects (5 women, 5 men, age 21-30 yr). High-resolution (0.2 mm in-plane) MRI scans at 7 Tesla were used for direct observation of the MCA diameter during hypocapnia, -1 kPa (-7.5 mmHg), normocapnia, 0 kPa (0 mmHg), and two levels of hypercapnia, +1 and +2 kPa (7.5 and 15 mmHg), with respect to baseline. The vessel lumen was manually delineated by two independent observers. The results showed that the MCA diameter increased by 6.8 ± 2.9% in response to 2 kPa end-tidal P(CO2) (PET(CO2)) above baseline. However, no significant changes in diameter were observed at the -1 kPa (-1.2 ± 2.4%), and +1 kPa (+1.4 ± 3.2%) levels relative to normocapnia. The nonlinear response of the MCA diameter to CO2 was fitted as a continuous calibration curve. Cerebral blood flow changes measured by transcranial Doppler could be corrected by this calibration curve using concomitant PET(CO2) measurements. In conclusion, the MCA diameter remains constant during small deviations of the PET(CO2) from normocapnia, but increases at higher PET(CO2) values.In the evaluation of cerebrovascular CO2 reactivity measurements, it is often assumed that the diameter of the large intracranial arteries insonated by transcranial Doppler remains unaffected by changes in arterial CO2 partial pressure. However, the strong cerebral vasodilatory capacity of CO2 challenges this assumption, suggesting that there should be some changes in diameter, even if very small. Data from previous studies on effects of CO2 on cerebral artery diameter [middle cerebral artery (MCA)] have been inconsistent. In this study, we examined 10 healthy subjects (5 women, 5 men, age 21-30 yr). High-resolution (0.2 mm in-plane) MRI scans at 7 Tesla were used for direct observation of the MCA diameter during hypocapnia, -1 kPa (-7.5 mmHg), normocapnia, 0 kPa (0 mmHg), and two levels of hypercapnia, +1 and +2 kPa (7.5 and 15 mmHg), with respect to baseline. The vessel lumen was manually delineated by two independent observers. The results showed that the MCA diameter increased by 6.8 ± 2.9% in response to 2 kPa end-tidal P(CO2) (PET(CO2)) above baseline. However, no significant changes in diameter were observed at the -1 kPa (-1.2 ± 2.4%), and +1 kPa (+1.4 ± 3.2%) levels relative to normocapnia. The nonlinear response of the MCA diameter to CO2 was fitted as a continuous calibration curve. Cerebral blood flow changes measured by transcranial Doppler could be corrected by this calibration curve using concomitant PET(CO2) measurements. In conclusion, the MCA diameter remains constant during small deviations of the PET(CO2) from normocapnia, but increases at higher PET(CO2) values. In the evaluation of cerebrovascular CO... reactivity measurements, it is often assumed that the diameter of the large intracranial arteries insonated by transcranial Doppler remains unaffected by changes in arterial CO... partial pressure. However, the strong cerebral vasodilatory capacity of CO... challenges this assumption, suggesting that there should be some changes in diameter, even if very small. Data from previous studies on effects of CO... on cerebral artery diameter [middle cerebral artery (MCA)] have been inconsistent. In this study, we examined 10 healthy subjects (5 women, 5 men, age 21-30 yr). High-resolution (0.2 mm in-plane) MRI scans at 7 Tesla were used for direct observation of the MCA diameter during hypocapnia, -1 kPa (-7.5 mmHg), normocapnia, 0 kPa (0 mmHg), and two levels of hypercapnia, +1 and +2 kPa (7.5 and 15 mmHg), with respect to baseline. The vessel lumen was manually delineated by two independent observers. The results showed that the MCA diameter increased by 6.8 plus or minus 2.9% in response to 2 kPa end-tidal Pco... (PetCO...) above baseline. However, no significant changes in diameter were observed at the -1 kPa (-1.2 plus or minus 2.4%), and +1 kPa (+1.4 plus or minus 3.2%) levels relative to normocapnia. The nonlinear response of the MCA diameter to CO2 was fitted as a continuous calibration curve. Cerebral blood flow changes measured by transcranial Doppler could be corrected by this calibration curve using concomitant PetCO... measurements. In conclusion, the MCA diameter remains constant during small deviations of the PetCO... from normocapnia, but increases at higher PetCO... values. (ProQuest: ... denotes formulae/symbols omitted.) In the evaluation of cerebrovascular CO 2 reactivity measurements, it is often assumed that the diameter of the large intracranial arteries insonated by transcranial Doppler remains unaffected by changes in arterial CO 2 partial pressure. However, the strong cerebral vasodilatory capacity of CO 2 challenges this assumption, suggesting that there should be some changes in diameter, even if very small. Data from previous studies on effects of CO 2 on cerebral artery diameter [middle cerebral artery (MCA)] have been inconsistent. In this study, we examined 10 healthy subjects (5 women, 5 men, age 21–30 yr). High-resolution (0.2 mm in-plane) MRI scans at 7 Tesla were used for direct observation of the MCA diameter during hypocapnia, −1 kPa (−7.5 mmHg), normocapnia, 0 kPa (0 mmHg), and two levels of hypercapnia, +1 and +2 kPa (7.5 and 15 mmHg), with respect to baseline. The vessel lumen was manually delineated by two independent observers. The results showed that the MCA diameter increased by 6.8 ± 2.9% in response to 2 kPa end-tidal Pco 2 (Pet CO 2 ) above baseline. However, no significant changes in diameter were observed at the −1 kPa (−1.2 ± 2.4%), and +1 kPa (+1.4 ± 3.2%) levels relative to normocapnia. The nonlinear response of the MCA diameter to CO 2 was fitted as a continuous calibration curve. Cerebral blood flow changes measured by transcranial Doppler could be corrected by this calibration curve using concomitant Pet CO 2 measurements. In conclusion, the MCA diameter remains constant during small deviations of the Pet CO 2 from normocapnia, but increases at higher Pet CO 2 values. In the evaluation of cerebrovascular CO... reactivity measurements, it is often assumed that the diameter of the large intracranial arteries insonated by transcranial Doppler remains unaffected by changes in arterial CO... partial pressure. However, the strong cerebral vasodilatory capacity of CO... challenges this assumption, suggesting that there should be some changes in diameter, even if very small. Data from previous studies on effects of CO... on cerebral artery diameter [middle cerebral artery (MCA)] have been inconsistent. In this study, we examined 10 healthy subjects (5 women, 5 men, age 21-30 yr). High-resolution (0.2 mm in-plane) MRI scans at 7 Tesla were used for direct observation of the MCA diameter during hypocapnia, -1 kPa (-7.5 mmHg), normocapnia, 0 kPa (0 mmHg), and two levels of hypercapnia, +1 and +2 kPa (7.5 and 15 mmHg), with respect to baseline. The vessel lumen was manually delineated by two independent observers. The results showed that the MCA diameter increased by 6.8 ± 2.9% in response to 2 kPa end-tidal Pco... (PetCO...) above baseline. However, no significant changes in diameter were observed at the -1 kPa (-1.2 ± 2.4%), and +1 kPa (+1.4 ± 3.2%) levels relative to normocapnia. The nonlinear response of the MCA diameter to CO2 was fitted as a continuous calibration curve. Cerebral blood flow changes measured by transcranial Doppler could be corrected by this calibration curve using concomitant PetCO... measurements. In conclusion, the MCA diameter remains constant during small deviations of the PetCO... from normocapnia, but increases at higher PetCO... values. (ProQuest: ... denotes formulae/symbols omitted.) In the evaluation of cerebrovascular CO2 reactivity measurements, it is often assumed that the diameter of the large intracranial arteries insonated by transcranial Doppler remains unaffected by changes in arterial CO2 partial pressure. However, the strong cerebral vasodilatory capacity of CO2 challenges this assumption, suggesting that there should be some changes in diameter, even if very small. Data from previous studies on effects of CO2 on cerebral artery diameter [middle cerebral artery (MCA)] have been inconsistent. In this study, we examined 10 healthy subjects (5 women, 5 men, age 21-30 yr). High-resolution (0.2 mm in-plane) MRI scans at 7 Tesla were used for direct observation of the MCA diameter during hypocapnia, -1 kPa (-7.5 mmHg), normocapnia, 0 kPa (0 mmHg), and two levels of hypercapnia, +1 and +2 kPa (7.5 and 15 mmHg), with respect to baseline. The vessel lumen was manually delineated by two independent observers. The results showed that the MCA diameter increased by 6.8 ± 2.9% in response to 2 kPa end-tidal P(CO2) (PET(CO2)) above baseline. However, no significant changes in diameter were observed at the -1 kPa (-1.2 ± 2.4%), and +1 kPa (+1.4 ± 3.2%) levels relative to normocapnia. The nonlinear response of the MCA diameter to CO2 was fitted as a continuous calibration curve. Cerebral blood flow changes measured by transcranial Doppler could be corrected by this calibration curve using concomitant PET(CO2) measurements. In conclusion, the MCA diameter remains constant during small deviations of the PET(CO2) from normocapnia, but increases at higher PET(CO2) values. |
| Author | Daemen, Mat J. A. P. Versluis, Maarten J. Ghariq, Eidrees Verbree, Jasper van Osch, Matthias J. P. Dahan, Albert Bronzwaer, Anne-Sophie G. T. van Buchem, Mark A. van Lieshout, Johannes J. |
| Author_xml | – sequence: 1 givenname: Jasper surname: Verbree fullname: Verbree, Jasper organization: Department of Radiology, Leiden University Medical Center, Leiden, The Netherlands;, C. J. Gorter Center for High Field MRI, Department of Radiology, Leiden University Medical Center, Leiden, The Netherlands – sequence: 2 givenname: Anne-Sophie G. T. surname: Bronzwaer fullname: Bronzwaer, Anne-Sophie G. T. organization: Laboratory for Clinical Cardiovascular Physiology, Academic Medical Center, Amsterdam, The Netherlands;, Department of Internal Medicine, Academic Medical Center, Amsterdam, The Netherlands; and – sequence: 3 givenname: Eidrees surname: Ghariq fullname: Ghariq, Eidrees organization: Department of Radiology, Leiden University Medical Center, Leiden, The Netherlands;, C. J. Gorter Center for High Field MRI, Department of Radiology, Leiden University Medical Center, Leiden, The Netherlands – sequence: 4 givenname: Maarten J. surname: Versluis fullname: Versluis, Maarten J. organization: Department of Radiology, Leiden University Medical Center, Leiden, The Netherlands;, C. J. Gorter Center for High Field MRI, Department of Radiology, Leiden University Medical Center, Leiden, The Netherlands – sequence: 5 givenname: Mat J. A. P. surname: Daemen fullname: Daemen, Mat J. A. P. organization: Department of Pathology, Academic Medical Center, Amsterdam, The Netherlands – sequence: 6 givenname: Mark A. surname: van Buchem fullname: van Buchem, Mark A. organization: Department of Radiology, Leiden University Medical Center, Leiden, The Netherlands – sequence: 7 givenname: Albert surname: Dahan fullname: Dahan, Albert organization: Department of Anesthesiology, Leiden University Medical Center, Leiden, The Netherlands – sequence: 8 givenname: Johannes J. surname: van Lieshout fullname: van Lieshout, Johannes J. organization: Laboratory for Clinical Cardiovascular Physiology, Academic Medical Center, Amsterdam, The Netherlands;, Department of Internal Medicine, Academic Medical Center, Amsterdam, The Netherlands; and, MRC/Arthritis Research UK Centre for Musculoskeletal Ageing Research, School of Life Sciences, University of Nottingham Medical School, Queen's Medical Centre, Nottingham, United Kingdom – sequence: 9 givenname: Matthias J. P. surname: van Osch fullname: van Osch, Matthias J. P. organization: Department of Radiology, Leiden University Medical Center, Leiden, The Netherlands;, C. J. Gorter Center for High Field MRI, Department of Radiology, Leiden University Medical Center, Leiden, The Netherlands |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/25190741$$D View this record in MEDLINE/PubMed |
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| Cites_doi | 10.1161/01.STR.20.1.45 10.1038/jcbfm.1984.54 10.1152/japplphysiol.00854.2014 10.1161/01.STR.30.1.81 10.1371/journal.pmed.0040239 10.1002/(SICI)1522-2594(199903)41:3<575::AID-MRM22>3.0.CO;2-W 10.1007/BF00327574 10.1113/jphysiol.2012.228551 10.1002/mrm.1910170215 10.1016/S0730-725X(01)00227-2 10.1113/jphysiol.2007.137075 10.1152/japplphysiol.90549.2008 10.1152/ajpregu.91008.2008 10.1016/S0952-8180(98)00107-X 10.1097/00004424-196701000-00016 10.1161/01.STR.27.12.2244 10.1152/japplphysiol.00637.2013 10.3174/ajnr.A2438 10.1161/01.STR.31.7.1672 10.1152/japplphysiol.91198.2008 10.1152/jappl.1996.81.3.1084 10.1227/00006123-199305000-00006 10.1161/01.STR.19.8.963 10.1007/BF01772826 |
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