Measuring global cerebrovascular pulsatility transmission using 4D flow MRI.

Pulse wave encephalopathy (PWE) is hypothesised to initiate many forms of dementia, motivating its identification and risk assessment. As candidate pulsatility based biomarkers for PWE, pulsatility index and pulsatility damping have been studied and, currently, do not adequately stratify risk due to variability in pulsatility and spatial bias. Here, we propose a locus-independent pulsatility transmission coefficient computed by spatially tracking pulsatility along vessels to characterise the brain pulse dynamics at a whole-organ level. Our preliminary analyses in a cohort of 20 subjects indicate that this measurement agrees with clinical observations relating blood pulsatility with age, heart rate, and sex, making it a suitable candidate to study the risk of PWE. We identified transmission differences between vascular regions perfused by the basilar and internal carotid arteries attributed to the identified dependence on cerebral blood flow, and some participants presented differences between the internal carotid perfused regions that were not related to flow or pulsatility burden, suggesting underlying mechanical differences. Large populational studies would benefit from retrospective pulsatility transmission analyses, providing a new comprehensive arterial description of the hemodynamic state in the brain. We provide a publicly available implementation of our tools to derive this coefficient, built into pre-existing open-source software.

Assessment of Dynamic Cerebral Autoregulation During Long-Term Exposure to High Altitude in Normal Subjects by Ultrasonography.

PURPOSE: To evaluate changes in dynamic cerebral autoregulation (CA) during short-term and long-term exposure to high altitude with ultrasonography, and also study the sex differences in the response of CA to altitude. METHODS: We assessed the differences in dynamic CA and measured with Doppler ultrasound of the bilateral internal carotid artery (ICA), vertebral artery (VA), and middle cerebral artery (MCA) and the values of basic information within 48 hours and at 2 years after arrival at Tibet in 65 healthy Han young Chinese volunteers, meanwhile, we compared the resistance index (RI) and pulsatility index (PI) of the right MCA at inhale oxygen 8 minutes when a newcomer with 2 years after arrival at Tibet. RESULTS: With 2 years of altitude exposure, the SaO2 of all subjects was above 90%, the mean PEF, DAP, and HR values decreased, HGB increased compared within 48 hours in same-gender groups. Comparisons of cerebral hemodynamics between before 2 years and after 2 years within male and female groups, the mean RI and PI values of bilateral MCA after 2 years were significantly higher than before 2 years, at the same time, the mean RI and PI values of bilateral ICA were significant differences (P < .05) between male groups, with regard to female groups, showed that the mean RI and PI values of bilateral VA were significant differences (P < .05). Comparisons of Right MCA hemodynamics between after oxygen uptake 8 minutes and 2 years, the mean RI and PI values were no significant difference within male and female groups (P > .05). CONCLUSIONS: Acute mountain sickness could result from an alteration of dynamic autoregulation of cerebral blood flow, but the impaired autoregulation may be corrected with the extension of time, furthermore, the response of CA to altitude in males and females are different.

Dynamic cerebral autoregulation is preserved during orthostasis and intrathoracic pressure regulation in healthy subjects: A pilot study.

Resistance breathing may restore cardiac output (CO) and cerebral blood flow (CBF) during hypovolemia. We assessed CBF and cerebral autoregulation (CA) during tilt, resistance breathing, and paced breathing in 10 healthy subjects. Blood velocities in the internal carotid artery (ICA), middle cerebral arteries (MCA, four subjects), and aorta were measured by Doppler ultrasound in 30° and 60° semi-recumbent positions. ICA blood flow and CO were calculated. Arterial blood pressure (ABP, Finometer), and end-tidal CO2 (ETCO2) were recorded. ICA blood flow response was assessed by mixed-models regression analysis. The synchronization index (SI) for the variable pairs ABP-ICA blood velocity, ABP-MCA velocities in 0.005-0.08 Hz frequency interval was calculated as a measure of CA. Passive tilting from 30° to 60° resulted in 12% decrease in CO (p = 0.001); ICA blood flow tended to fall (p = 0.04); Resistance breathing restored CO and ICA blood flow despite a 10% ETCO2 drop. ETCO2 and CO contributed to ICA blood flow variance (adjusted R2: 0.9, p < 0.0001). The median SI was low (<0.2) indicating intact CA, confirmed by surrogate date testing. The peak SI was transiently elevated during resistance breathing in the 60° position. Resistance breathing may transiently reduce CA efficiency. Paced breathing did not restore CO or ICA blood flow.

Quantification of neurovascular compliance with retrospectively gated phase-contrast MRI.

OBJECTIVE: Neurovascular compliance (NVC) is the change in the brain's arterial tree blood volume, ΔV, divided by the change in intra-vascular blood pressure, ΔP, during the cardiac cycle. The primary aim of this work was to evaluate the performance of MRI measurement of NVC obtained from time-resolved measurements of internal carotid artery (ICA) and vertebral artery (VA) flow rates. A secondary aim was to explore whether NVC could be estimated from common carotid (CCA) flow in conjunction with prior knowledge of mean ICA and VA fractional flow rates, given the small cross-section of ICA and VA in some populations, in particular small children. METHODS: ΔV was quantified from the blood flow rate measured at the ICA and VA for actual NVC derivation. It was further estimated from individually measured CCA flow rate and mean flow fractions ICA/CCA and VA/CCA (which could alternatively be obtained from literature data), to yield estimated NVC. Time-resolved blood flow rate in CCA, ICA and VA was obtained via retrospectively-gated 2D PC-MRI at 1.5 T in healthy subjects (N = 16, 8 women, mean age 36 ± 13 years). ΔP was determined via a brachial pressure measurement. RESULTS: Actual and estimated mean NVC were 27 ± 15 and 38 ± 15 µL/mmHg, respectively, and the two measurements were strongly correlated (r = 0.80; p = 0.0002) with test-retest intra-class correlation coefficients of 0.964 and 0.899. CONCLUSION: Both methods yielded excellent retest precision. In spite of a large bias, actual and estimated NVC were strongly correlated.

Handgrip exercise does not alter CO2 -mediated cerebrovascular flow-mediated dilation.

Handgrip exercise (HG), a small muscle exercise, improves cognitive function and is expected to provide a useful exercise mode to maintain cerebral health. However, the effect of HG on cerebral blood flow regulation is not fully understood. The present study aimed to examine the effect of acute HG on cerebral endothelial function as one of the essential cerebral blood flow regulatory functions. Thirteen healthy young participants performed interval HG, consisting of 4 sets of 2 min HG at 25% of maximum voluntary contraction with 3 min recovery between each set. Cognitive performance was evaluated before and at 5 and 60 min after interval HG using the Go/No-Go task (reaction time and accuracy). The diameter and blood velocity of the internal carotid artery (ICA) were measured using a duplex Doppler ultrasound system. To assess cerebral endothelial function, hypercapnia (30 s of hypercapnia stimulation, end-tidal partial pressure of CO2 : +9 mmHg)-induced cerebrovascular flow-mediated dilatation (cFMD) was induced, calculated as relative peak dilatation from baseline diameter. The shear rate (SR) was calculated using the diameter and blood velocity of the ICA. As a result, cognitive performance improved only at 5 min after interval HG (reaction time, P = 0.008; accuracy, P = 0.186), whereas ICA SR during interval HG and cFMD after interval HG were unchanged (P = 0.313 and P = 0.440, respectively). These results suggest that enhancement in cerebral endothelial function is not an essential mechanism responsible for acute HG-induced cognitive improvement. NEW FINDINGS: What is the central question of this study? Does handgrip exercise, a small muscle exercise, improve cerebral endothelial function? What is the main finding and its importance? Acute interval isometric handgrip exercise (2 min of exercise at 25% maximum voluntary contraction, followed by 3 min of recovery, repeated for a total of 4 sets) did not improve cerebral endothelial function. Since the cerebrovascular shear rate did not change during exercise, it is possible that acute handgrip exercise is not sufficient stimulation to improve cerebral endothelial function.

Selective elevation in external carotid artery flow during acute gravitational transition to microgravity during parabolic flight.

This study sought to determine to what extent acute exposure to microgravity (0 G) and related increases in central blood volume (CBV) during parabolic flight influence the regional redistribution of intra and extra cranial cerebral blood flow (CBF). Eleven healthy participants performed during two parabolic flights campaigns aboard the Airbus A310-ZERO G aircraft. The response of select variables for each of the 15 parabolas involving exposure to both 0 G and hypergravity (1.8 G) were assessed in the seated position. Mean arterial blood pressure (MAP) and heart rate (HR) were continuously monitored and used to calculate stroke volume (SV), cardiac output ([Formula: see text]), and systemic vascular resistance (SVR). Changes in CBV were measured using an impedance monitor. Extracranial flow through the internal carotid, external carotid, and vertebral artery ([Formula: see text]ICA, [Formula: see text]ECA, and [Formula: see text]VA), and intracranial blood velocity was measured by duplex ultrasound. When compared with 1-G baseline condition, 0 G increased CBV (+375 ± 98 mL, P = 0.004) and [Formula: see text] (+16 ± 14%, P = 0.024) and decreased SVR (-7.3 ± 5 mmHg·min·L-1, P = 0.002) and MAP (-13 ± 4 mmHg, P = 0.001). [Formula: see text]ECA increased by 43 ± 46% in 0 G (P = 0.030), whereas no change was observed for CBF, [Formula: see text]ICA, or [Formula: see text]VA (P = 0.102, P = 0.637, and P = 0.095, respectively).NEW & NOTEWORTHY Our findings demonstrate that in microgravity there is a selective increase in external carotid artery blood flow whereas global and regional cerebral blood flow remained preserved. To what extent this reflects an adaptive, neuroprotective response to counter overperfusion remains to be established.

Shear stress metrics associated with pro-atherogenic high-risk anatomical features in a carotid artery bifurcation model.

BACKGROUND: Diseases associated with atherosclerotic plaques in the carotid artery are a major cause of deaths in the United States. Blood-flow-induced shear-stresses are known to trigger plaque formation. Prior literature suggests that the internal carotid artery sinus is prone to atherosclerosis, but there is limited understanding of why only certain patients are predisposed towards plaque formation. METHODS: We computationally investigate the effect of vessel geometry on wall-shear-stress distribution by comparing flowfields and wall-shear-stress-metrics between a low-risk and a novel predisposed high-risk carotid artery bifurcation anatomy. Both models were developed based on clinical risk estimations and patient-averaged anatomical features. The high-risk geometry has a larger internal carotid artery branching angle and a lower internal-to-carotid-artery-diameter-ratio. A patient-averaged physiological carotid artery inflow waveform is used. FINDINGS: The high-risk geometry experiences stronger flow separation in the sinus. Furthermore, it experiences a more equal flow split at the bifurcation, thereby reducing internal carotid artery flowrate and increasing atherosclerosis-prone low-velocity areas. Lowest time-averaged-wall-shear-stresses are present at the sinus outer wall, where plaques are often found, for both geometries. The high-risk geometry has significantly high, unfavorable oscillatory-shear-index values not found in the low-risk geometry. High oscillatory-shear-index areas are located at the vessels outside walls distal to the bifurcation and on the sinus wall. INTERPRETATION: These results highlight the effectiveness of oscillatory-shear-index, to augment classical time-averaged-wall-shear-stress, in evaluating pro-atherogenic geometry features. Furthermore, the flow split at the bifurcation is a promising clinical indicator for atherosclerosis risk as it can be directly accessed using clinical imaging, whereas shear-stress-metrics cannot.

Dynamic resistance exercise-induced pressor response does not alter hypercapnia-induced cerebral vasodilation in young adults.

Excessive arterial pressure elevation induced by resistance exercise (RE) attenuates peripheral vasodilatory function, but its effect on cerebrovascular function is unknown. We aimed to evaluate the effect of different pressor responses to RE on hypercapnia-induced vasodilation of the internal carotid artery (ICA), an index of cerebrovascular function. To manipulate pressor responses to RE, 15 healthy young adults (11M/4F) performed two RE: high intensity with low repetitions (HL) and low intensity with high repetitions (LH) dynamic knee extension. ICA dilation, induced by 3 min of hypercapnia, was measured before and 10 min after RE using Doppler ultrasound. HL exercise elicited a greater pressor response than LH exercise. In relaxation phases of RE, ICA blood velocity increased in both HL and LH trials. However, ICA shear rate did not significantly increase in either trial (P = 0.06). Consequently, neither exercise altered post-exercise hypercapnia-induced ICA dilation (HL, 3.9 ± 1.9% to 5.1 ± 1.7%; LH, 4.6 ± 1.4% to 4.8 ± 1.8%; P > 0.05 for all). When viewed individually, the changes in ICA shear rate were positively correlated with changes in end-tidal partial pressure of carbon dioxide (PETCO2) (r = 0.46, P < 0.01) than with mean arterial pressure (r = 0.32, P = 0.02). These findings suggest that the effects of RE-induced pressor response on cerebrovascular function may be different from peripheral arteries. An increase in PETCO2 during the relaxation phase may play a more crucial role than elevated pressure in increasing cerebral shear during dynamic RE.

Cerebral endothelium-dependent function and reactivity to hypercapnia: the role of α1-adrenoreceptors.

We assessed hypercapnic cerebrovascular reactivity (CVR) and endothelium-dependent function [cerebral shear-mediated dilation (cSMD)] in the internal carotid artery (ICA) with and without systemic α1-adrenoreceptor blockade via Prazosin. We hypothesized that CVR would be reduced, whereas cSMD would remain unchanged, after Prazosin administration when compared with placebo. In 15 healthy adults (3 female, 26 ± 4 years), we conducted ICA duplex ultrasound during CVR [target +10 mmHg partial pressure of end-tidal carbon dioxide ([Formula: see text]) above baseline, 5 min] and cSMD (+9 mmHg [Formula: see text] above baseline, 30 s) using dynamic end-tidal forcing with and without α1-adrenergic blockade (Prazosin; 0.05 mg/kg) in a placebo-controlled, double-blind, and randomized design. The CVR in the ICA was not different between placebo and Prazosin (P = 0.578). During CVR, the reactivities of mean arterial pressure and cerebrovascular conductance to hypercapnia were also not different between conditions (P = 0.921 and P = 0.664, respectively). During Prazosin, cSMD was lower (1.1 ± 2.0% vs 3.8 ± 3.0%; P = 0.032); however, these data should be interpreted with caution due to the elevated baseline diameter (+1.3 ± 3.6%; condition: P = 0.0498) and lower shear rate (-14.5 ± 23.0%; condition: P < 0.001). Therefore, lower cSMD post α1-adrenoreceptor blockade might not indicate a reduction in cerebral endothelial function per se, but rather, that α1-adrenoreceptors contribute to resting cerebral vascular restraint at the level of the ICA.NEW & NOTEWORTHY We assessed steady-state hypercapnic cerebrovascular reactivity and cerebral endothelium-dependent function, with and without α1-adrenergic blockade (Prazosin), in a placebo-controlled, double-blind, and randomized study, to assess the contribution of α1-adrenergic receptors to cerebrovascular CO2 regulation. After administration of Prazosin, cerebrovascular reactivity to CO2 was not different compared with placebo despite lower blood flow, whereas cerebral endothelium-dependent function was reduced, likely due to elevated baseline internal carotid arterial diameter. These findings suggest that α1-adrenoreceptor activity does not influence cerebral blood flow regulation to CO2 and cerebral endothelial function.

Response of internal carotid artery blood flow velocity to fluid challenge under general anesthesia in pediatric patients with moyamoya disease: A prospective observational study.

BACKGROUND: Maintaining cerebral blood flow is important in intraoperative management of moyamoya disease patients. AIMS: To access changes in the carotid artery blood flow velocity in response to fluid challenge, blood pressure, and cardiac output under general anesthesia in pediatric patients with moyamoya disease. METHODS: This observational study included pediatric patients with moyamoya disease undergoing general anesthesia for encephaloduroarteriosynangiosis. Each patient underwent an ultrasound assessment thrice as follows: after anesthetic induction (T1), after fluid challenge (10 ml/kg, T2), and at the end of surgery (T3). The primary outcome was the change in the internal carotid artery blood flow velocity after fluid challenge and was assessed using a paired t-test. The secondary outcomes comprised changes in the internal, external, and common carotid artery blood flow peak velocities after fluid challenge and the factors influencing these changes. RESULTS: We enrolled and analyzed 30 patients with a mean age of 7.2 years. After fluid challenge, the systolic (p = .003) and mean blood pressure (p = .017), stroke volume index (p = .008), and cardiac index (p = .140) were higher than those at T1. However, both internal carotid artery blood flow velocities did not change after fluid challenge (p = .798, mean difference and 95% confidence interval [CI], -1.1 and -10.3 to 8.0 for right, p = .164, mean difference and 95% CI, -5.2 and -12.7 to 2.2 for left). The internal carotid artery blood flow velocity was correlated with the cardiac index, stroke volume index, and mean and diastolic blood pressure, with low significance. CONCLUSIONS: The internal carotid artery blood flow velocity did not increase in pediatric patients with moyamoya disease under general anesthesia, despite fluid challenge and corresponding changes in the blood pressure and cardiac output. Intraoperative hemodynamic management to improve the cerebral blood flow in these patients requires further investigation.

Dynamic onset response of the internal carotid artery to hypercapnia is blunted in children compared with adults.

Intracranial blood velocity reactivity to a steady-state hypercapnic stimulus has been shown to be similar in children and adults, but the onset response to hypercapnia is slower in the child. Given the vasodilatory effect of hypercapnia on the cerebrovasculature, assessment of vessel diameter, and blood flow are vital to fully elucidate whether the temporal hypercapnic response differs in children versus adults. Assessment of internal carotid artery (ICA) vessel diameter (ICAd), blood velocity (ICAv), volumetric blood flow (QICA ), and shear rate (ICASR ) in response to a 4 min hypercapnic challenge was completed in children (n = 14, 8 girls; 9.8 ± 0.7 years) and adults (n = 17, 7 females; 24.7 ± 1.8 years). The dynamic onset responses of partial pressure of end-tidal CO2 (PET CO2 ), QICA , ICAv, and ICASR to hypercapnia were modeled, and mean response time (MRT) was computed. Following 4 min of hypercapnia, ICA reactivity and ICAd were comparable between the groups. Despite a similar MRT in PET CO2 in children and adults, children had slower QICA (children 108 ± 60 s vs. adults 66 ± 37 s; p = 0.023), ICAv (children 120 ± 52 s vs. adults 52 ± 31 s; p = 0.001), and ICASR (children 90 ± 27 s vs. adults 47 ± 36 s; p = 0.001) MRTs compared with adults. This is the first study to show slower hypercapnic hyperemic kinetic responses of the ICA in children. The mechanisms determining these differences and the need to consider the duration of hypercapnic exposure when assessing CVR in children should be considered in future studies.

Plasticity of the bony carotid canal and its clinical use for assessing negative remodeling of the internal carotid artery.

BACKGROUND AND OBJECTIVE: It has long been believed that the bony carotid canal has no plasticity and that a small canal represents a hypoplastic internal carotid artery. We aimed to show whether the carotid canal can narrow according to morphological changes in the internal carotid artery. MATERIALS AND METHODS: The carotid canal diameter was longitudinally measured in seven individuals who underwent carotid artery ligation. As moyamoya disease is known to be associated with negative remodeling of the internal carotid artery, the carotid canal diameter was measured in 106 patients with moyamoya disease, and an association with the outer diameter of the internal carotid artery or a correlation with the disease stage was investigated. The carotid canal was measured by computed tomography (106 patients), and the outer diameter of the artery was measured by high-resolution magnetic resonance imaging (63 patients). The carotid canal area was calculated by the product of the maximum axial diameter and its perpendicular diameter. RESULTS: All seven patients who underwent carotid artery ligation showed narrowing of the carotid canal, and the carotid canal area decreased by 12.2%-28.9% during a mean follow-up period of 4.2 years. In patients with moyamoya disease, the carotid canal area showed a linear correlation with the outer area of the internal carotid artery (r = 0.657, p < 0.001), and a negative correlation with the disease stage (ρ = -0.283, p < 0.001). CONCLUSION: The bony carotid canal has plasticity, and its area reflects the outer area of the internal carotid artery, therefore, it can be used to assess the remodeling of the carotid artery. A narrow carotid canal may not necessarily indicate hypoplastic internal carotid artery.

Resistance, but not endurance exercise training, induces changes in cerebrovascular function in healthy young subjects.

It is generally considered that regular exercise maintains brain health and reduces the risk of cerebrovascular diseases such as stroke and dementia. Since the benefits of different "types" of exercise are unclear, we sought to compare the impacts of endurance and resistance training on cerebrovascular function. In a randomized and crossover design, 68 young healthy adults were recruited to participate in 3 mo of resistance and endurance training. Cerebral hemodynamics through the internal carotid, vertebral, middle and posterior cerebral arteries were measured using Duplex ultrasound and transcranial Doppler at rest and during acute exercise, dynamic autoregulation, and cerebrovascular reactivity (to hypercapnia). Following resistance, but not endurance training, middle cerebral artery velocity and pulsatility index significantly decreased (P < 0.01 and P = 0.02, respectively), whereas mean arterial pressure and indices of cerebrovascular resistance in the middle, posterior, and internal carotid arteries all increased (P < 0.05). Cerebrovascular resistance indices in response to acute exercise and hypercapnia also significantly increased following resistance (P = 0.02), but not endurance training. Our findings, which were consistent across multiple domains of cerebrovascular function, suggest that episodic increases in arterial pressure associated with resistance training may increase cerebrovascular resistance. The implications of long-term resistance training on brain health require future study, especially in populations with pre-existing cerebral hypoperfusion and/or hypotension.NEW & NOTEWORTHY Three months of endurance exercise did not elicit adaptation in any domain of cerebrovascular function in young healthy inactive volunteers. However, resistance training induced decreased pulsatility in the extracranial arteries and increased indices of cerebrovascular resistance in cerebral arteries. This increase in cerebrovascular resistance, apparent at baseline and in response to both hypercapnia and acute exercise, may reflect a protective response in the face of changes in arterial pressure during resistance exercise.

The regional effect of serum hormone levels on cerebral blood flow in healthy nonpregnant women.

Sex hormones estrogen (EST) and progesterone (PROG) have received increased attention for their important physiological action outside of reproduction. While studies have shown that EST and PROG have significant impacts on brain function, their impact on the cerebrovascular system in humans remains largely unknown. To address this, we used a multi-modal magnetic resonance imaging (MRI) approach to investigate the link between serum hormones in the follicular phase and luteal phase of the menstrual cycle (MC) with measures of cerebrovascular function (cerebral blood flow [CBF]) and structure (intracranial artery diameter). Fourteen naturally cycling women were recruited and assessed at two-time points of their MC. CBF was derived from pseudo-continuous arterial spin labeling while diameters of the internal carotid and basilar artery was assessed using time of flight magnetic resonance angiography, blood samples were performed after the MRI. Results show that PROG and EST had opposing and spatially distinct effects on CBF: PROG correlated negatively with CBF in anterior brain regions (r = -.86, p < .01), while EST correlations were positive, yet weak and most prominent in posterior areas (r = .78, p < .01). No significant correlations between either hormone or intracranial artery diameter were observed. These results show that EST and PROG have opposing and regionally distinct effects on CBF and that this relationship is likely not due to interactions with large intracranial arteries. Considering that CBF in healthy women appears tightly linked to their current hormonal state, future studies should consider assessing MC-related hormone fluctuations in the design of functional MRI studies in this population.

The carotid axis revisited.

The aim was to determine the variations in the level of origin of carotid bifurcation and diameters of the common, internal, and external carotid arteries which is clinically important for several interventional procedures. Therefore, 165 human embalmed corpses were dissected. The data collected were analyzed using the Chi square-test and the Pearson correlation test. The results of previous studies have been reviewed. In relation to the level of the carotid bifurcation, taking as a reference point the hyoid bone, the values ranged from 4 cm below the hyoid body to 2.5 cm above the body of the hyoid, being the average height-0.33 cm, with a standard deviation of 1.19 cm. The right carotid bifurcation was established at a higher level (x = - 0.19 cm.) than the left one (x = - 0.48 cm.) (p = 0.046). On the contrary, no significant gender differences could be observed. The arterial calibres of the common and internal carotid arteries were higher in male than female. In the internal carotid artery (X = 0.76 cm.), the left was greater than the right (X = 0.72 cm.) (P = 0.047). However, no differences in the distribution of the calibre of the external carotid artery were found neither by side nor gender. Variations in the level of bifurcation and calibres of carotid arteries are relevant for interventional radiology procedures and head and neck surgeries. Knowledge of these anatomical references might help clinicians in the interpretation of the carotid system.

Cortical thinning is associated with brain pulsatility in older adults: An MRI and NIRS study.

Aging is accompanied by global brain atrophy occurring unequally across the brain. Cortical thinning is seen with aging with a larger loss in the frontal and temporal subregions. We explored the link between regional cortical thickness and regional cerebral pulsatility. Sixty healthy individuals were divided into two age groups, young (aged 19-31) and older (aged 65-75) adults. Each participant underwent a near-infrared spectroscopy (NIRS) scan to index regional brain pulsatility from cerebral pulse-transit-time-to-the peak-of-the-pulse (PTTp), an anatomical magnetic resonance imaging (MRI) and a phase-contrast MRI (PC-MRI) scan to measure arterial and cerebrospinal fluid (CSF) pulsatility. In older adults, the greatest association between cerebral pulsatility and cortical thickness was found in superior and middle temporal and superior, middle and inferior frontal areas, which are the regions perfused first by the internal carotid arteries. This association dropped in the postcentral and superior parietal regions. These findings suggest higher brain pulsatility as a potential risk factor contributing to cortical thinning for some brain regions more than others.

High-but not moderate-intensity exercise acutely attenuates hypercapnia-induced vasodilation of the internal carotid artery in young men.

PURPOSE: Exercise-induced increases in shear rate (SR) across different exercise intensities may differentially affect hypercapnia-induced vasodilation of the internal carotid artery (ICA), a potential index of cerebrovascular function. We aimed to elucidate the effects of exercise intensity on ICA SR during exercise and post-exercise hypercapnia-induced vasodilation of the ICA in young men. METHODS: Twelve healthy men completed 30 min of cycling at moderate [MIE; 65 ± 5% of age-predicted maximal heart rate (HRmax)] and high (HIE; 85 ± 5% HRmax) intensities. Hypercapnia-induced vasodilation was induced by 3 min of hypercapnia (target end-tidal partial pressure of CO2 + 10 mmHg) and was assessed at pre-exercise, 5 min and 60 min after exercise. Doppler ultrasound was used to measure ICA diameter and blood velocity during exercise and hypercapnia tests. RESULTS: SR was not altered during either exercise (interaction and main effects of time; both P > 0.05). ICA conductance decreased during HIE from resting values (5.1 ± 1.3 to 3.2 ± 1.0 mL·min-1·mmHg-1; P < 0.01) but not during MIE (5.0 ± 1.3 to 4.0 ± 0.8 mL·min-1·mmHg-1; P = 0.11). Consequently, hypercapnia-induced vasodilation declined immediately after HIE (6.9 ± 1.7% to 4.0 ± 1.4%; P < 0.01), but not after MIE (7.2 ± 2.1% to 7.3 ± 1.8%; P > 0.05). Sixty minutes after exercise, hypercapnia-induced vasodilation returned to baseline values in both trials (MIE 8.0 ± 3.1%; HIE 6.4 ± 2.9%; both P > 0.05). CONCLUSION: The present study showed blunted hypercapnia-induced vasodilation of the ICA immediately after high-intensity exercise, but not a moderate-intensity exercise in young men. Given that the acute response is partly linked to the adaptive response in the peripheral endothelial function, the effects of aerobic training on cerebrovascular health may vary depending on exercise intensity.

Bilateral regional extracranial blood flow regulation to hypoxia and unilateral duplex ultrasound measurement error.

NEW FINDINGS: What is the central question of this study? Is blood flow regulation to hypoxia different between the internal carotid arteries (ICAs) and vertebral arteries (VAs), and what is the measurement error in unilateral extracranial artery assessments compared to bilateral? What is the main finding and its importance? ICA and VA blood flow regulation to hypoxia is comparable when factoring for vessel type and vessel side. Compared to bilateral assessment, vessels assessed unilaterally had individual measurement errors of up to 37%. Assessing the vessel with the larger resting blood flow, not the left or right vessel, reduces unilateral measurement error. ABSTRACT: Whether blood flow regulation to hypoxia is similar between left and right internal carotid arteries (ICAs) and vertebral arteries (VAs) is unclear. Extracranial blood flow is regularly calculated by doubling a unilateral assessment; however, lateral artery differences may lead to measurement error. This study aimed to determine extracranial blood flow regulation to hypoxia when factoring for vessel type (ICAs or VAs) and vessel side (left or right) effects, and to investigate unilateral assessment measurement error compared to bilateral assessment. In a repeated-measures crossover design, extracranial arteries of 44 participants were assessed bilaterally by duplex ultrasound during 90 min of normoxic and poikilocapnic hypoxic (12.0% fraction of inspired oxygen) conditions. Linear mixed model analyses revealed no Condition × Vessel Type × Vessel Side interaction for blood flow, vessel diameter and flow velocity (all P > 0.05) indicating left and right ICA and VA blood flow regulation to hypoxia was similar. Bilateral hypoxic reactivity was comparable (ICAs, 1.4 (1.0) vs. VAs, 1.7 (1.1) Δ%·Δ SpO2-1 ; P = 0.12). Compared to bilateral assessment, unilateral mean measurement error of the relative blood flow response to hypoxia was up to 5%, but individual errors reached 37% and were greatest in ICAs and VAs with the smaller resting blood flow due to a ratio-scaling problem. In conclusion, left and right ICA and VA regulation to hypoxia is comparable when factoring for vessel type and vessel side. Assessing the ICA and VA vessels with the larger resting blood flow, not the left or right vessel, reduces unilateral measurement error.

Effects of head position on internal and external carotid pressures in standing sedated horses.

The effects of head position on internal carotid artery (ICA) and external carotid artery (ECA) pressures in standing sedated horses were evaluated in this study. The common carotid artery (CCA) was catheterized in 6 horses using an ultrasound-guided technique to facilitate placement of a pressure transducer within the ICA and ECA at the level of the guttural pouch. Transducer position was confirmed by endoscopic visualization. Mean arterial pressure (MAP) was measured with horses in both a head-up and head-down position. The dorsal metatarsal artery was catheterized as a control. Maintaining a head-up position decreased MAP in both the ICA (median: 75.21 mmHg) and ECA (median: 79.43 mmHg), relative to the head-down position (ICA median: 104.65 mmHg; ECA median: 102.26 mmHg). Mean arterial pressure in the dorsal metatarsal artery was not affected by head position. The head-up position resulted in lower arterial pressures in both the ICA and ECA (P = 0.03) compared with the head-down position in standing sedated horses.

Cette étude a évalué les effets de la position de la tête sur la pression artérielle au niveau de l'artère carotide interne (ICA) et de l'artère carotide externe (ECA) chez des chevaux sous sedation debout. L'artère carotide commune (CCA) a été cathétérisée chez six chevaux en utilisant une technique échoguidée pour faciliter le placement d'un transducteur de pression dans l'ICA et l'ECA au niveau de la poche gutturale. La position du transducteur a été confirmée par endoscopie. La pression artérielle moyenne (MAP) a été mesurée chez les chevaux avec la tête en position haute et en position basse. L'artère métatarsienne dorsale a été cathétérisée et a servi comme témoin. Les MAP enregistrées au niveau de l'ICA (médiane: 75,21 mmHg) et de l'ECA (médiane: 79,43 mmHg) lorsque la tête est en position élevée sont plus faibles que celles enregistrées lorsque la tête est en position basse (médiane ICA: 104,65 mmHg; médiane ECA: 102,26 mmHg). La MAP de l'artère métatarsienne dorsale n'a pas été affectée par la position de la tête. En conclusion, chez les chevaux sédatés et debout, la position élevée de la tête produit des pressions artérielles plus faibles au niveau de ICA et ECA (P = 0,03) que celles obtenues lorsque la tête est en position basse.(Traduit par les auteurs).

Parasympathetic brainstem origin sites of triggered external and internal carotid vasodilation are not distributed topographically in the rat.

Cranial parasympathetic activation produces vasodilation in the head and neck region, but little is known about its central and peripheral mechanisms. This study was conducted to examine whether external and internal carotid-vasodilation origin sites triggered by chemical stimulation are distributed topographically in the parasympathetic brainstems of anesthetized rats, and to examine the effects of peripheral receptors on vasodilation. Microinjection of the neuromodulator candidate l-cysteine revealed that external and internal carotid vasodilation-triggering sites were distributed non-topographically along the full extent of the parasympathetic parvocellular reticular formation (PcRt). Intravenous injection of a muscarinic blocker and a nitric oxide synthase inhibitor abolished external carotid vasodilation, suggesting the peripheral involvement of muscarinic and nitric oxide receptors. Further work is needed to fully understand the PcRt mechanisms underlying timely and appropriate vasodilation to support various cranial functions.