MRI Measures of Middle Cerebral Artery Diameter in Conscious Humans During Simulated Orthostasis

Serrador, Jorge M.; Picot, Paul A.; Rutt, Brian K.; Shoemaker, J. Kevin; Bondar, Roberta L.

doi:10.1161/01.str.31.7.1672

Cited by 644 publications

(551 citation statements)

References 53 publications

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“…We used Doppler ultrasound to measure flow velocity, rather than blood flow, in MCA; nevertheless, earlier reports indicate that MCAv is a reliable index of CBF during both changes in arterial PCO 2 45-47 and orthostatic stress. 48 Finally, the NIRS monitors oxygenation in tissue and confirms the capillary-oxygen-level-dependent related increase in oxygenation observed by functional magnetic resonance imaging during neural activation. 49 We acknowledge that NIRS measures only local (that is to one depth) oxygenation and that discreet regions of the brain may respond differently during orthostatic stress.…”

Section: Methodological Considerationssupporting

confidence: 53%

Identical pattern of cerebral hypoperfusion during different types of syncope

et al. 2009

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Syncope is caused by insufficient oxygen supply to the brain. There have been attempts to classify syncope on the basis of defects in the venous system, arterial system (that is impaired systemic vascular resistance) or a combination of the two (that is mixed). We examined the hypothesis that a comparable decrease in cerebral perfusion would be evident at pre-syncope irrespective of the category of dysfunction. Young healthy volunteers (N ¼ 37) participated. The protocol consisted of 15 min supine rest, followed by 601 head-up tilt and lower body suction in increments of À10 mm Hg for 5 min each until pre-syncope. Beat-to-beat blood pressure (BP) (Finometer or intra-arterial), cardiac output (Finometer), middle cerebral artery blood velocity (MCAv), end-tidal CO 2 and cerebral oxygenation were monitored continuously. At pre-syncope, mixed dysfunction was common (21 out of 37 participants), followed by venular dysfunction (15 out of 37 participants). In the venular and mixed groups, comparable orthostatic tolerance and declines in BP (À37 vs À43% from baseline, respectively), end-tidal PCO 2 , MCAv (À35 vs À38%) and cerebral oxygenation (À5 vs À7%) were evident despite distinct mechanisms purportedly being responsible for the hypotension. Although different determinants of hypotension do exist, cerebral hypoperfusion occurs to a similar extent.

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Section: Methodological Considerationssupporting

confidence: 53%

Identical pattern of cerebral hypoperfusion during different types of syncope

et al. 2009

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“…This assumption is only valid if the diameter of the insonated vessel remains constant. Measurements of MCA diameters in humans have shown that the diameters do not change during alterations in PET CO 2 (14,36). Therefore, it is likely that alterations in MCA V mean reflect changes in cerebral blood flow in the present study.…”

Section: Limitationsmentioning

confidence: 60%

“…These combined responses are likely to be key mechanisms responsible for reductions in orthostatic tolerance in heat-stressed individuals, although the cause(s) by which heat stress alters cerebral vascular responses is not entirely clear. Given the close relationship between cerebral perfusion and Pa CO 2 (16,36), decreases in Pa CO 2 (as reflected by decreases in PET CO 2 ) that occur during heat stress alone and combined heat and orthostatic stress (40,41) could account for passive heat stress-induced reductions in resting cerebral blood flow and augmented decreases in CBVC during combined orthostatic and heat stress. However, based on the previously reported relationship that every 1-Torr change in Pa CO 2 changes cerebral blood flow ϳ3% in the same direction under normothermic conditions (31), the decreases in PET CO 2 that are evident during heat and combined heat and orthostatic stresses are not large enough to fully account for all of the decrease in cerebral blood flow.…”

Section: Discussionmentioning

confidence: 99%

“…Although mechanisms responsible for reduced orthostatic tolerance during heat stress are unclear, they are likely associated with factors that directly or indirectly affect cerebral perfusion pressure, cerebral blood flow, and thus cerebral oxygenation (20,24,38). Cerebral perfusion is very sensitive to changes in arterial carbon dioxide tension (Pa CO 2 ), such that increases in Pa CO 2 increase cerebral perfusion, whereas decreases in Pa CO 2 decrease cerebral perfusion (16,36). Previously, our laboratory identified decreases in end-tidal carbon dioxide (PET CO 2 ; surrogate of Pa CO 2 ) of ϳ2 Torr in response to whole body passive heat stress, as well as significant reductions in cerebral perfusion and cerebral vascular conductance (40,41).…”

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confidence: 99%

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Cerebrovascular responsiveness to steady-state changes in end-tidal CO₂ during passive heat stress

Low

Wingo

Keller

et al. 2008

Journal of Applied Physiology

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CG. Cerebrovascular responsiveness to steady-state changes in end-tidal CO2 during passive heat stress. J Appl Physiol 104: 976-981, 2008. First published January 24, 2008 doi:10.1152/japplphysiol.01040.2007.-This study tested the hypothesis that passive heat stress alters cerebrovascular responsiveness to steady-state changes in end-tidal CO2 (PETCO 2 ). Nine healthy subjects (4 men and 5 women), each dressed in a water-perfused suit, underwent normoxic hypocapnic hyperventilation (decrease PETCO 2 ϳ20 Torr) and normoxic hypercapnic (increase in PETCO 2 ϳ9 Torr) challenges under normothermic and passive heat stress conditions. The slope of the relationship between calculated cerebrovascular conductance (CBVC; middle cerebral artery blood velocity/mean arterial blood pressure) and PETCO 2 was used to evaluate cerebrovascular CO2 responsiveness. Passive heat stress increased core temperature (1.1 Ϯ 0.2°C, P Ͻ 0.001) and reduced middle cerebral artery blood velocity by 8 Ϯ 8 cm/s (P ϭ 0.01), reduced CBVC by 0.09 Ϯ 0.09 CBVC units (P ϭ 0.02), and decreased PETCO 2 by 3 Ϯ 4 Torr (P ϭ 0.07), while mean arterial blood pressure was well maintained (P ϭ 0.36). The slope of the CBVC-PET CO 2 relationship to the hypocapnic challenge was not different between normothermia and heat stress conditions (0.009 Ϯ 0.006 vs. 0.009 Ϯ 0.004 CBVC units/Torr, P ϭ 0.63). Similarly, in response to the hypercapnic challenge, the slope of the CBVC-PETCO 2 relationship was not different between normothermia and heat stress conditions (0.028 Ϯ 0.020 vs. 0.023 Ϯ 0.008 CBVC units/Torr, P ϭ 0.31). These results indicate that cerebrovascular CO2 responsiveness, to the prescribed steady-state changes in PETCO 2 , is unchanged during passive heat stress. brain blood flow; hyperthermia; hypocapnia; hypercapnia ORTHOSTATIC TOLERANCE IS REDUCED under heat stress, relative to normothermic, conditions (1,8,19,40,41). Although mechanisms responsible for reduced orthostatic tolerance during heat stress are unclear, they are likely associated with factors that directly or indirectly affect cerebral perfusion pressure, cerebral blood flow, and thus cerebral oxygenation (20, 24,38). Cerebral perfusion is very sensitive to changes in arterial carbon dioxide tension (Pa CO 2 ), such that increases in Pa CO 2 increase cerebral perfusion, whereas decreases in Pa CO 2 decrease cerebral perfusion (16, 36). Previously, our laboratory identified decreases in end-tidal carbon dioxide (PET CO 2 ; surrogate of Pa CO 2 ) of ϳ2 Torr in response to whole body passive heat stress, as well as significant reductions in cerebral perfusion and cerebral vascular conductance (40,41). Decreased cerebral perfusion would theoretically reduce the functional reserve by which cerebral blood flow can decrease further, before the onset of syncopal symptoms.It is unlikely that the relatively small decrease in PET CO 2 (i.e., ϳ2 Torr) in response to passive heat stress is the sole mechanism leading to the observed reduction in cerebral perfusion. However, this assumption is based on ca...

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“…Any changes in arterial diameter can introduce errors in the estimation of flow. Though Serrador et al40 demonstrated that the diameter of the MCA does not change in humans at the level of measurement during hyper/hypocapnia or during moderate hypotension, the effects of BP changes on MCA diameter have not been fully investigated 41. Finally, we did not measure central PP; rather, we measured PP from the radial artery.…”

Section: Discussionmentioning

confidence: 95%

Relationship Between the Ambulatory Arterial Stiffness Index and the Lower Limit of Cerebral Autoregulation During Cardiac Surgery

Obata

Barodka

Berkowitz

et al. 2018

JAHA

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BackgroundPulse pressure, the ambulatory arterial stiffness index (AASI), and the symmetric AASI are established predictors of adverse cardiovascular outcomes. However, little is known about their relationship to cerebral autoregulation. This study evaluated whether these markers of vascular properties relate to the lower limit of cerebral autoregulation (LLA).Methods and ResultsThe LLA was determined during cardiac surgery with transcranial Doppler ultrasonography in 181 patients. All other variables were calculated from continuous intraoperative readings obtained before cardiopulmonary bypass. The LLA varied directly with the AASI (β=3.12 per 0.1 change in AASI, P<0.001) and to a lesser extent the symmetric AASI (β=2.02 per 0.1 change in symmetric AASI, P≤0.022), while peripheral pulse pressure was not significantly related (β=0.0, P>0.99). Logistic regression revealed that the likelihood of LLA being >65 mm Hg increased by 50% (95% confidence interval, 11%–102%, P=0.008) for every 0.1 increase in the AASI. The AASI was able to predict a LLA above certain thresholds (area under the curve receiver operating characteristic for AASI predicting an LLA >65 mm Hg: 0.60; 95% confidence interval, 0.51%–0.68%, P=0.043). Incorporating additional variables improved the model's predictive ability (area under the curve for AASI predicting a LLA >65 mm Hg: 0.75; 95% confidence interval, 0.68–0.82, P=0.036).ConclusionsThese data indicate that the LLA is related to the mechanical properties of the vasculature as represented by the AASI. The AASI can be used to predict LLA threshold levels during cardiac surgery. It is now possible to link elevations in the LLA with an increased AASI as determined from readily accessible intraoperative variables.

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MRI Measures of Middle Cerebral Artery Diameter in Conscious Humans During Simulated Orthostasis

Cited by 644 publications

References 53 publications

Identical pattern of cerebral hypoperfusion during different types of syncope

Identical pattern of cerebral hypoperfusion during different types of syncope

Cerebrovascular responsiveness to steady-state changes in end-tidal CO₂ during passive heat stress

Relationship Between the Ambulatory Arterial Stiffness Index and the Lower Limit of Cerebral Autoregulation During Cardiac Surgery

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