Internal Carotid Artery Blood Flow Research Articles

Internal carotid artery blood flow is enhanced by elevating blood pressure during combined propofol-remifentanil and thoracic epidural anaesthesia

Anaesthesia reduces mean arterial pressure (MAP), and to preserve organ perfusion, vasopressors are often used to maintain MAP above 60 mmHg. Cognitive dysfunction is common following major surgery and may relate to intra-operative cerebral hypoperfusion. The aim of this study was to evaluate whether internal carotid artery (ICA) blood flow increases when MAP is kept higher than 60 mmHg using noradrenaline. A randomised, cross-over trial. Department of Anaesthesia, Rigshospitalet, Copenhagen, Denmark, from December 2017 to April 2018. Patients with median [IQR] age 71 [63 to 75] years underwent pancreaticoduodenectomy (n = 19), total pancreatic resection (n = 1) or gastro-entero anastomosis (n = 2) during combined propofol-remifentanil and thoracic epidural anaesthesia. MAP was maintained between 60 to 65, 70 to 75 and 80 to 85 mmHg, in a random order, by noradrenaline infusion at a stable level of anaesthesia. Primary outcome was change in ICA flow at MAP 60 to 65 vs. 80 to 85 mmHg. Secondary outcomes were change in ICA flow at MAP 60 to 65 vs. 70 to 75 and 70 to 75 vs. 80 to 85 mmHg. Duplex ultrasound evaluated ICA flow. A (mean ± SD) increase in MAP from 62 ± 1 to 82 ± 1 mmHg elevated ICA flow from 196 ± 53 to 226 ± 61 ml min (mean difference 31 ml min; 95% CI 19 to 42; P < 0.0001). An increase in MAP from 62 ± 1 to 72 ± 1 mmHg elevated ICA flow to 210 ± 52 ml min (P = 0.0271) and ICA flow increased further (P = 0.0165) when MAP was elevated to 82 ± 1 mmHg. During combined propofol-remifentanil and thoracic epidural anaesthesia, ICA flow increased by approximately 15% when the MAP was elevated from about 60 to 80 mmHg. Treatment of a reduction in MAP brought about by anaesthesia seems to enhance ICA flow. Clinicaltrials.gov ID: NCT03309917.

Effects of Cervical Rotation Angle on Atherosclerotic Internal Carotid Artery Blood Flow: A Safety Study Using an Animal Model of Internal Carotid Atherosclerosis

ObjectiveThe aim of this study was to investigate the effects of the cervical rotation angle (CRA) on atherosclerotic internal carotid artery blood flow (ICA-BF) in an animal model. MethodsThirty healthy New Zealand white rabbits were included in the study. Twenty of the 30 rabbits were chosen randomly to be the model rabbits, and the remaining 10 were chosen to be the normal rabbits. The model rabbits’ left ICAs were treated by atherosclerosis modeling. The left ICAs of the model rabbits with atherosclerotic stenosis were chosen as the experimental group, and the right ICAs of the model rabbits without atherosclerotic stenosis were chosen as the control group. The left ICAs of the normal rabbits were chosen as the blank group. Using color duplex ultrasound, ICA-BF was measured in the artery contralateral to the direction of rotation in the positions of neutral (Pre-0°), 15°, 30°, 45°, 60°, 75°, 90°, and subsequent neutral (Post-0°). ResultsStatistically significant decreases were seen in ICA-BF after cervical spine rotation (from Pre-0° to 90°) in the control group only (P < .05). All the values of end-diastolic velocity in the experimental group were lower than those in the blank group at the same CRAs. The resistance index and pulsatility index of the experimental group were higher than those of the blank group except at 45° rotation. ConclusionIn our animal model, in the rabbits with hyperlipidemia but without atherosclerotic stenosis, CRA had the greatest impact on ICA-BF. Furthermore, at some of the same CRAs (especially neutral, 30°, and 60°), there were statistical differences in ICA-BF among the 3 groups.

Resuscitative endovascular balloon occlusion of the aorta in zone I versus zone III in a porcine model of non-traumatic cardiac arrest and cardiopulmonary resuscitation: A randomized study

IntroductionResuscitative endovascular balloon occlusion of the aorta (REBOA) in zone I increases systemic blood pressure during cardiopulmonary resuscitation (CPR), while also obstructing the blood flow to distal organs. The aim of the study was to compare the effects on systemic blood pressure and visceral blood flow of REBOA-III (zone III, infrarenal) and REBOA-I (zone I, supraceliac) during non-traumatic cardiac arrest and CPR. MethodsCardiac arrest was induced in 61 anesthetized pigs. Thirty-two pigs were allocated to a hemodynamic study group where the primary outcomes were systemic arterial pressures and 29 pigs were allocated to a blood flow study group where the primary outcomes were superior mesenteric arterial (SMA) and internal carotid arterial (ICA) blood flow. After 7–8 min of CPR with a mechanical compression device, REBOA-I, REBOA-III or no aortic occlusion (control group) were initiated after randomization. ResultsSystemic mean and diastolic arterial pressures were statistically higher during CPR with REBOA-I compared to REBOA-III (50 mmHg and 16 mmHg in REBOA-I vs 38 mmHg and 1 mmHg in REBOA-III). Systemic systolic, mean and diastolic arterial pressures were statistically elevated during CPR in the REBOA-I group compared to the controls. The SMA blood flow increased by 49% in REBOA-III but dropped to the levels of the controls within minutes. The ICA blood flow increased the most in REBOA-I compared to REBOA-III and the control group (54%, 19% and 0%, respectively). ConclusionIn experimental non-traumatic cardiac arrest and CPR, REBOA-I increased systemic blood pressures more than REBOA-III, and the potential enhancement of visceral organ blood flow by REBOA-III was short-lived.

Cerebrovascular Reactivity in Young Adults with Major Depressive Disorder

Cerebral vasodilatory responsiveness is blunted in older adults (~70 yrs) with depressive disorders and thought to contribute to the link between depressive symptomology and increased risk for neurocognitive (e.g., dementia) and cerebral vascular (e.g., stroke) diseases. In young adults with major depressive disorder (MDD), peripheral vascular endothelial dysfunction is evident; however, to date, limited investigations have examined cerebral vasodilatory function in young otherwise healthy adults with MDD. We tested the hypothesis that cerebral vasodilatory responsiveness to a hypercapnic stimulus would be blunted in otherwise healthy young adults with MDD compared to healthy non‐depressed adults (HA). Four HA (22±2yrs) and 6 adults with MDD (23±2yrs; n=2 tested during a major depressive episode) participated. Beat‐to‐beat mean arterial pressure (MAP; finger photoplethysmography), middle cerebral artery blood velocity (MCAv; transcranial Doppler ultrasound), internal carotid artery (ICA) diameter and blood flow (Doppler ultrasound), and end‐tidal carbon dioxide concentration (PETCO2; capnograph) were continuously measured during baseline (i.e., normocapnia) and rebreathing‐induced hypercapnia. Cerebral vascular conductance index (CVCi=MCAv•MAP−1) and ICA blood flow (Vmean•π(d•20−1)2•60) and conductance (CVC=ICA blood flow•MAP−1) were calculated at baseline and at the highest common magnitude of hypercapnia achieved by all subjects during rebreathing (ΔPETCO2 = 9 Torr). At baseline, there were no differences in any outcome variable between groups (all p&gt;0.05). During hypercapnia, there were no group differences in the increase in MAP (Δ3±3 HA vs. Δ3±4 mmHg MDD; p=0.98). The increase in MCAv was blunted in adults with MDD (Δ33±4 HA vs. Δ23±7 cm•s−1 MDD; p=0.03). Both the absolute (Δ0.30±0.02 HA vs. Δ0.20±0.07 cm•s−1•mmHg−1 MDD; p=0.01) and relative (Δ42±7 HA vs. Δ26±9 %baseline MDD; p=0.01) increase in CVCi during hypercapnia were reduced in adults with MDD. There were no group differences in ICA diameter (Δ−0.04±0.22 HA vs. Δ0.05±0.17 mm MDD; p=0.51) or blood flow responses (Δ143±20 HA vs. Δ127±95 mL•min−1 MDD; p=0.49). Although the dilatory response in the ICA was ~50% less in adults with MDD, the increase in CVC was not significantly different between groups (Δ51±26 HA vs. Δ27±22 %baseline MDD; p=0.17). In adults with MDD, there was no relation between habitual physical activity and cerebral vasodilatory responsiveness (R2=0.09; p=0.57). These preliminary data suggest that cerebral vasodilatory reactivity to a hypercapnic stimulus may be blunted in young otherwise healthy adults with MDD, providing further support for the potential mechanistic link between cerebrovascular dysfunction and depression in increased neurocognitive and cerebral vascular disease risk.Support or Funding InformationHL133414 (JLG)

White Mountain Expedition 2019: The Impact of Sustained Hypoxia on Cerebral Blood Flow Responses and Tolerance to Simulated Hemorrhage

IntroductionTrauma‐induced hemorrhage can occur at high altitude from a variety of causes, including battlefield injuries, motor vehicle accidents, air accidents, and major falls. The hypoxic environment of high altitude can limit the ability of the cardiovascular system to compensate for blood loss injuries, due, in part, to the reduced arterial oxygen content. In humans, the effect of sustained hypoxia on tolerance to hemorrhage and the cardiovascular and cerebrovascular responses to this stress are unknown. Based on the known compensatory increases in cerebral blood flow that occur with exposure to hypoxia, we hypothesized that tolerance to simulated hemorrhage (via application of lower body negative pressure, LBNP) at high altitude would be similar compared to low altitude due to increased cerebral blood flow and oxygen delivery, and the subsequent preservation of cerebral tissue oxygenation.MethodsHealthy human subjects (N=8; 4F, 4M) participated in LBNP protocols to presyncope at low altitude (1045 m, Calgary, Canada) and at high altitude (3800 m, White Mountain, California) following 4–5 days of acclimatization. LBNP chamber pressure was initially reduced to −60 mmHg for 10‐min followed by decreases every 5‐min to −70, −80, −90 and −100 mmHg, until the onset of presyncopal symptoms. Arterial pressure, heart rate, internal carotid artery blood flow, and cerebral oxygen saturation were measured continuously. Stroke volume was derived from the arterial pressure waveform, and systemic vascular resistance was calculated from cardiac output and mean arterial pressure. Time to presyncope and cardiovascular responses were compared between the low and high altitude conditions.ResultsTime to presyncope was similar between conditions (low altitude: 1276 ± 108 s vs. high altitude: 1208± 108 s; P=0.58). Similar responses to LBNP were observed between low and high altitudes in mean arterial pressure (low altitude: −16±2 % vs. high altitude: −16±2 %; P=0.85), stroke volume (low altitude: −57±5 % vs. high altitude: −60±5 %; P=0.39), systemic vascular resistance (low altitude: +23±9 % vs. high altitude: +38±12 %; P=0.21), and heart rate (low altitude: +69±12 % vs. high altitude: +65±8 %; P=0.71). Internal carotid artery blood flow was higher at high altitude vs. low altitude (condition effect, P=0.01), and decreased with LBNP under both conditions (P≤0.005). There was no effect of high altitude on cerebral oxygen saturation at baseline and presyncope (altitude Effect, P=0.73).ConclusionThese findings suggest that the hypoxia induced by ascent to high altitude (3800 m) does not affect tolerance to simulated hemorrhage in young healthy adults, which may be due to 1) similar cardiovascular reflex responses to central hypovolemia, and/or 2) the compensatory increase in cerebral blood flow and subsequent maintenance of oxygen delivery to the tissues, resulting in the preservation of cerebral oxygen saturation.Support or Funding InformationAHA 17GRNT33671110

Internal carotid artery blood flow response to cognitive task is similar between young and older adults

Previous studies reported that the increase in the middle cerebral artery blood flow velocity during cognitive task was greater in older adults than in young adults, suggesting age‐related differences in cerebral blood flow responses to cognitive task. However, previous studies utilized transcranial Doppler ultrasound and thereby information regarding arterial diameter, blood volume flow, and vascular conductance was lacking. On the other hand, Doppler ultrasonography can assess blood volume flow in the internal carotid artery (ICA), which provides the blood supply to a large portion of the cerebral cortex. To date, it remains to be determined whether ICA blood flow response to cognitive task is different between young and older adults. The present study examined the ICA blood flow and blood pressure (BP) responses to 20 s of task switching in 6 young (30 ± 3 yr) and 6 older (66 ± 3 yr) subjects. The ICA blood flow and BP did not change significantly during task switching in young subjects. In older subjects, significant ICA blood flow response was not found, while BP increased (p&lt;0.05) slightly and transiently during the first 10 s of the task. In both subjects, vascular conductance of the ICA was unaltered during task switching. Our present findings suggest that the ICA blood flow response to task switching was similar between young and older subjects.Support or Funding InformationGrant‐in‐Aid for Research Activity start‐up from the Japan Society for the Promotion of Science (19K24333)

Cerebral Blood Flow and Cerebral Tissue Oxygen Responses to Inspiratory Resistance Breathing During Hypoxia

Increasing resistance to inspiration further decreases intrathoracic and intracranial pressures, leading to increases in venous return, stroke volume, and consequently, arterial pressure and cerebral perfusion pressure. Accordingly, inspiratory resistance breathing may be of therapeutic interest for clinical conditions associated with decreased delivery of blood and oxygen to the brain. Previous studies in healthy humans have investigated the effect of inspiratory resistance breathing on the cerebral circulation, by studying blood velocity within intracranial vessels (via transcranial Doppler (TCD) ultrasound), with equivocal results. The aim of this study was to investigate the effect of inspiratory resistance breathing on blood flow through the internal carotid artery (ICA), and cerebral tissue oxygenation during hypoxia. We hypothesized that inspiratory resistance breathing would increase ICA blood flow, and improve cerebral tissue oxygenation during a mild hypoxic stimulus.MethodsSix healthy human subjects (5M/1F) completed two 10‐min protocols in randomized order: 1) breathing a hypoxic gas mix (16% O2, balance N2), and 2) breathing a hypoxic gas mix (16% O2, balance N2) with inspiratory resistance of −7 cmH2O. ICA blood flow was derived from simultaneous measurements of blood velocity and diameter measured by duplex ultrasound, middle cerebral artery velocity (MCAv) was recorded continuously by TCD ultrasound, and cerebral tissue oxygenation (ScO2) was recorded by near‐infrared spectroscopy. Arterial oxygen saturation (SpO2) was measured by pulse oximetry, and end‐tidal O2 (etO2) was measured by a gas analyzer. Data were analyzed from the last 1‐min of baseline and each protocol with a linear mixed model.ResultsThe hypoxic stimulus decreased SpO2 and etO2 (P&lt;0.0001), and inspiratory resistance breathing did not protect against these responses (P≥0.21). ICA diameter increased with hypoxia under both conditions (P=0.002), regardless of resistance breathing (P=0.56). ICA velocity (23.6 ± 1.6 cm/s vs. 25.7 ± 1.1 cm/s) and flow (298.8 ± 36.6 ml/min vs. 328.8 ± 39.5 ml/min) were lower with hypoxia and inspiratory resistance breathing compared with hypoxia alone (P≤0.07), while mean MCAv was not affected by either hypoxia or resistance breathing (P≥0.15). ScO2 decreased under both conditions (P=0.0009; hypoxia: −2.7 ± 0.9 %; hypoxia + resistance breathing: −3.6 ± 0.8 %), with no effect of inspiratory resistance breathing (P=0.90).ConclusionThese preliminary data demonstrate that, contrary to our hypothesis, inspiratory resistance breathing did not increase ICA blood flow, nor improve cerebral tissue oxygenation during a mild hypoxic stimulus. Rather, ICA blood flow decreased with inspiratory resistance breathing during hypoxia, primarily due to a reduction in ICA blood velocity. Further studies are required to elucidate whether inspiratory resistance breathing may be of therapeutic interest for clinical conditions affecting cerebral blood flow and tissue oxygenation.

White Mountain Expedition 2019: Peaks and Valleys ‐ Oscillatory cerebral blood flow at high altitude

IntroductionCerebral tissue oxygenation can be impaired by decreases in oxygen delivery as a result of reduced cerebral blood flow, and environmental conditions such as ascent to high altitude. Recent evidence suggests that an oscillatory pattern in cerebral blood flow (at ~0.1 Hz) may protect cerebral oxygenation under conditions of cerebral hypoperfusion. In this study, we hypothesized that inducing oscillations in cerebral blood flow at 0.1 Hz would protect cerebral blood flow and cerebral tissue oxygen saturation during exposure to combined simulated hemorrhage and sustained hypobaric hypoxia (ascent and partial acclimatization to high altitude).Methods8 healthy human subjects (4 M, 24.7 ± 4.1 y; 4 F, 34.3 ± 8.3 y) participated in two experiments at high altitude (White Mountain, California, USA; altitude, 3800 m): 1) a control condition (CTRL) where lower body negative pressure (LBNP) was used to induce central hypovolemia by reducing chamber pressure to −60 mmHg for 10‐min, and 2) oscillatory LBNP (OLBNP) where chamber pressure was reduced to −60 mmHg, then oscillated every 5‐s between −30 mmHg and −90 mmHg for 10‐min (0.1 Hz). Measurements included internal carotid artery (ICA) blood flow via duplex Doppler ultrasound, middle cerebral artery velocity (MCAv) via transcranial Doppler ultrasound, and cerebral tissue oxygen saturation via near‐infrared spectroscopy. Frequency analysis (via fast Fourier transform) was performed to verify that oscillations in mean MCAv were generated at ~0.1 Hz. Data were analyzed with a linear mixed‐model. All data are represented as mean ± SE.ResultsLow frequency power (0.07–0.15 Hz) in mean MCAv increased during OLBNP vs. CTRL (P = 0.02). OLBNP did not protect ICA flow (OLBNP: −32.5 ± 4.5 Δ%; CTRL: −19.9 ± 8.9 Δ%; P = 0.18) or mean MCAv (OLBNP: −18.5 ± 3.4 Δ%; CTRL: −15.3 ± 5.4 Δ%; P = 0.58), but cerebral tissue oxygenation was protected (OLBNP: −0.67 ± 1.0 Δ%; CTRL: −4.07 ± 2.0 Δ%; P = 0.004).ConclusionsThese results support our hypothesis that inducing oscillatory blood flow leads to protection of cerebral tissue oxygenation, despite no differences in ICA blood flow or mean MCAv. Overall, these data suggest that therapies using oscillatory perfusion may help preserve cerebral tissue oxygen saturation under conditions of reduced oxygen delivery.Support or Funding InformationAHA 17GRNT33671110

Cerebrovascular reactivity to carbon dioxide is not influenced by variability in the ventilatory sensitivity to carbon dioxide.

What is the central question of this study? Do differing magnitudes of ventilation influence cerebrovascular CO2 reactivity and the cerebral blood flow response to increases in arterial carbon dioxide? What is the main finding and its importance? While a greater ventilation, through voluntary hyperventilation, is associated with a higher anterior cerebral blood flow during carbon dioxide breathing, this elevated cerebral blood flow is due to a higher blood pressure and not ventilation per se. A greater ventilation, through voluntary hyperventilation, does not influence global or posterior cerebral blood flow during carbon dioxide breathing. Cerebrovascular reactivity to carbon dioxide is not influenced by an individual's ventilatory sensitivity to carbon dioxide. Recent work demonstrated an influence of ventilation on cerebrovascular reactivity to CO2 ; however, the concomitant influence of changes in mean arterial blood pressure (MAP) on ventilation-induced differences in cerebral blood flow (CBF) has yet to be examined in this context. Healthy participants (n=15; 25±3years of age; 179±6cm height; 74±10kg weight; 3 female) underwent end-tidal forcing to increase their partial pressure of end-tidal CO2 by +3, +6 and +9mmHg above baseline in 5-min sequential steps while maintaining iso-oxia. This protocol was then repeated twice, with participants hyperventilating and hypoventilating by ∼30% compared to the first trial. Intra-cranial and extra-cranial CBF were measured using ultrasound. The MAP (finger photo-plethysmography) was higher during the hyperventilation and hypoventilation trials compared to normal ventilation (main effects, P<0.05 for both). While internal carotid artery blood flow was higher during the hyperventilation trial compared to normal ventilation (P=0.01), this was due to a higher MAP, as indicated by analysis of conductance values (P=0.68) or inclusion of MAP in covariate analysis (P=0.11). Global CBF (P=0.11) and vertebral artery blood flow (P=0.93) were unaffected by the magnitude of ventilation. Further, CO2 reactivity was not affected by the different breathing trials (P>0.05 for all). Retrospective analysis of a larger data set (n=53) confirmed these observations and demonstrated no relationships between the ventilatory and global CBF response to hypercapnia (r2 =0.04; P=0.14). Therefore, when differences in MAP are accounted for, cerebrovascular CO2 reactivity (assessed via end-tidal forcing) is independent of the magnitude of ventilation.

Arterial and venous cerebral blood flow responses to long-term head-down bed rest in male volunteers.

What is the central question of this study? A heterogeneous cerebral blood flow (CBF) response in the cerebral arteries has been demonstrated in several physiological conditions, and it might be attributable to different physiological properties. However, the whole cerebral haemodynamic response to weightlessness remains unknown. What is the main finding and its importance? Long-term head-down bed rest caused a heterogeneous CBF response between the anterior and posterior cerebral arteries and between the cerebral arteries and veins. Especially, in contrast to the anterior cerebral circulation, the posterior arterial and venous CBFs were well maintained throughout weightlessness. In this study, we investigated the whole cerebral haemodynamic response to long-term head-down bed rest (HDBR). We hypothesized that long-term exposure to weightlessness influences cerebral blood flow (CBF) or CBF distribution among cerebral arteries and veins because of the different physiological roles of each cerebral vessel. To test this hypothesis, 10 male volunteers were exposed to -6deg HDBR for 60days. Blood flows in the internal carotid artery, external carotid artery and vertebral artery or internal jugular vein and vertebral vein were measured using ultrasonography before and on days30 and 57 of the HDBR. The internal carotid artery blood flow was reduced on day30 (P=0.019) and had returned to the baseline level by day57. In contrast, the vertebral artery blood flow remained unaltered throughout the HDBR (P=0.626). The internal jugular vein blood flow was reduced on day30 (P=0.009), whereas the vertebral vein blood flow remained unaltered (P=0.397). These findings suggest that long-term HDBR causes a heterogeneous CBF response between the anterior and posterior cerebral circulation in the both arteries and veins. The posterior arterial and venous CBFs were well maintained throughout HDBR, and these CBF responses to HDBR were different from the anterior cerebral circulation.

Cerebral blood flow responses to exercise are enhanced in left ventricular assist device patients after an exercise rehabilitation program.

Cerebral blood flow during exercise is impaired in patients with heart failure implanted with left ventricular assist devices (LVADs). Our aim was to determine whether a 3-mo exercise training program could mitigate cerebrovascular dysfunction. Internal carotid artery (ICA) blood flow and intracranial middle (MCAv) and posterior cerebral (PCAv) artery velocities were measured continuously using Doppler ultrasound, alongside cardiorespiratory measures at rest and in response to an incremental cycle ergometer exercise protocol in 12 LVAD participants (5 female, 53.6 ± 11.8 yr; 84.2 ± 15.7 kg; 1.73 ± 0.08) pre- (PreTR) and post- (PostTR) completion of a 3-mo supervised exercise rehabilitation program. At rest, only PCAv was different PostTR (38.1 ± 10.4 cm/s) compared with PreTR (43.0 ± 10.8 cm/s; P < 0.05). PreTR, the reduction in PCAv observed from rest to exercise (5.2 ± 1.8%) was mitigated PostTR (P < 0.001). Similarly, exercise training enhanced ICA flow during submaximal exercise (~8.6 ± 13.7%), resulting in increased ICA flow PostTR compared with a reduced flow PreTR (P < 0.001). Although both end-tidal partial pressure of carbon dioxide and mean arterial pressure responses during incremental exercise were greater PostTR than PreTR, only the improved was related to the improved ICA flow (R2 = 0.14; P < 0.05). Our findings suggest that short-term exercise training improves cerebrovascular function during exercise in patients with LVADs. This finding should encourage future studies investigating long-term exercise training and cerebral and peripheral vascular adaptation.NEW & NOTEWORTHY Left ventricular assist devices, now used as destination therapy in end-stage heart failure, enable patients to undertake rehabilitative exercise training. We show, for the first time in humans, that training improves cerebrovascular function during exercise in patients with left ventricular assist devices. This finding may have implications for cerebrovascular health in patients with heart failure.

Differential vasomotor responses to isocapnic hyperoxia: cerebral versus peripheral circulation.

Isocapnic hyperoxia (IH) evokes cerebral and peripheral hypoperfusion via both disturbance of redox homeostasis and reduction in nitric oxide (NO) bioavailability. However, it is not clear whether the magnitude of the vasomotor responses depends on the vessel network exposed to IH. To test the hypothesis that the magnitude of IH-induced reduction in peripheral blood flow (BF) may differ from the hypoperfusion response observed in the cerebral vascular network under oxygen-enriched conditions, nine healthy men (25 ± 3 yr, mean ± SD) underwent 10 min of IH during either saline or vitamin C (3 g) infusion, separately. Femoral artery (FA), internal carotid artery (ICA), and vertebral artery (VA) BF (Doppler ultrasound), as well as arterial oxidant (8-isoprostane), antioxidant [ascorbic acid (AA)], and NO bioavailability (nitrite) markers were simultaneously measured. IH increased 8-isoprostane levels and reduced nitrite levels; these responses were followed by a reduction in both FA BF and ICA BF, whereas VA BF did not change. Absolute and relative reductions in FA BF were greater than IH-induced changes in ICA and VA perfusion. Vitamin C infusion increased arterial AA levels and abolished the IH-induced increase in 8-isoprostane levels and reduction in nitrite levels. Whereas ICA and VA BF did not change during the vitamin C-IH trial, FA perfusion increased and reached similar levels to those observed during normoxia with saline infusion. Therefore, the magnitude of IH-induced reduction in femoral blood flow is greater than that observed in the vessel network of the brain, which might involve the determinant contribution that NO has in the regulation of peripheral vascular perfusion.

Internal Carotid Artery Blood Flow in Pediatric Moyamoya Patients

Internal Carotid Artery Blood Flow in Pediatric Moyamoya Patients

Internal Carotid Artery Blood Flow Response to Anesthesia, Pneumoperitoneum, and Head-up Tilt during Laparoscopic Cholecystectomy.

Little is known about how implementation of pneumoperitoneum and head-up tilt position contributes to general anesthesia-induced decrease in cerebral blood flow in humans. We investigated this question in patients undergoing laparoscopic cholecystectomy, hypothesizing that cardiorespiratory changes during this procedure would reduce cerebral perfusion. In a nonrandomized, observational study of 16 patients (American Society of Anesthesiologists physical status I or II) undergoing laparoscopic cholecystectomy, internal carotid artery blood velocity was measured by Doppler ultrasound at four time points: awake, after anesthesia induction, after induction of pneumoperitoneum, and after head-up tilt. Vessel diameter was obtained each time, and internal carotid artery blood flow, the main outcome variable, was calculated. The authors recorded pulse contour estimated mean arterial blood pressure (MAP), heart rate (HR), stroke volume (SV) index, cardiac index, end-tidal carbon dioxide (ETCO2), bispectral index, and ventilator settings. Results are medians (95% CI). Internal carotid artery blood flow decreased upon anesthesia induction from 350 ml/min (273 to 410) to 213 ml/min (175 to 249; -37%, P < 0.001), and tended to decrease further with pneumoperitoneum (178 ml/min [127 to 208], -15%, P = 0.026). Tilt induced no further change (171 ml/min [134 to 205]). ETCO2 and bispectral index were unchanged after induction. MAP decreased with anesthesia, from 102 (91 to 108) to 72 (65 to 76) mmHg, and then remained unchanged (Pneumoperitoneum: 70 [63 to 75]; Tilt: 74 [66 to 78]). Cardiac index decreased with anesthesia and with pneumoperitoneum (overall from 3.2 [2.7 to 3.5] to 2.3 [1.9 to 2.5] l · min · m); tilt induced no further change (2.1 [1.8 to 2.3]). Multiple regression analysis attributed the fall in internal carotid artery blood flow to reduced cardiac index (both HR and SV index contributing) and MAP (P < 0.001). Vessel diameter also declined (P < 0.01). During laparoscopic cholecystectomy, internal carotid artery blood flow declined with anesthesia and with pneumoperitoneum, in close association with reductions in cardiac index and MAP. Head-up tilt caused no further reduction. Cardiac output independently affects human cerebral blood flow.

Safety and Clinical Efficacy of Yangxue Qingnao Granules in the Treatment of Chronic Cerebral Circulation Insufficiency: A Systematic Review and Meta-Analysis.

To evaluate the safety and clinical efficacy of Yangxue Qingnao (YXQN) granules in the treatment of chronic cerebral circulation insufficiency (CCCI), electronic databases—PubMed, Embase, CNKI, VIP, and Wangfang—were searched for randomized controlled trials (RCTs) published up to January 2019. GRADE and RevMan 5.3.0 were used for grading and analysis, respectively. Fifteen trials involving 1211 CCCI patients were included. Subgroup analysis was performed owing to study heterogeneity. Compared to nimodipine plus routine treatment, YXQN granules plus routine treatment were more effective in increasing basilar artery (BA) blood flow velocity (mean difference (MD) = 3.34, 95% confidence interval (CI) = [2.31, 4.37], P < 0.00001), vertebral artery (VA) blood flow velocity (MD = 0.52, 95% CI = [0.27, 0.76], P < 0.0001), and internal carotid artery (ICA) blood flow velocity (MD = 7.46, 95% CI = [2.01, 12.90], P=0.007). In improving the clinical efficacy of traditional Chinese medicine (TCM) for symptoms such as headache, dizziness, and insomnia, YXQN granules plus routine treatment were shown to be superior to the following control treatments: nimodipine plus routine treatment (mean difference (M-H) = 4.21, 95% CI = [2.49, 7.12], P < 0.00001), flunarizine plus routine treatment (mean difference (M-H) = 3.92, 95% CI = [1.36, 11.29], P=0.01), troxerutin plus routine treatment (mean difference (M-H) = 4.79, 95% CI = [2.20, 10.42], P < 0.00001), and routine treatment (mean difference (M-H) = 6.13, 95% CI = [1.48, 25.34], P=0.01). Risk of bias was assessed in 15 trials. One analysis was graded using GRADE and showed poor results. Adverse events were not reported explicitly in all but one trial. Thus, this meta-analysis suggests that YXQN granules may be beneficial for patients with CCCI. However, owing to the poor quality of the clinical trials and small sample sizes, a definite conclusion on the efficacy and safety of YXQN granules cannot be drawn from existing information.

Dynamic assessment of cerebral blood flow and intracranial pressure during inversion table tilt using ultrasonography

ContextInversion tables are used as treatment for back pain, but there is a lack of agreement on systemic effects of inversion. ObjectiveTo assess intracranial pressure (ICP) and cerebral blood flow using ultrasonography during inversion table tilt. MethodsOptic nerve sheath diameter (ONSD), heart rate (HR), blood pressure, internal carotid artery (ICA) and middle cerebral artery (MCA) blood flow of participants were measured in 3 positions: supine before inversion, during inversion with head down, and supine post-inversion. ONSD was evaluated with ocular ultrasonography and blood flow (ICA and MCA) with Doppler ultrasonography. ResultsThe ONSD changed significantly between the supine position, at 3 min of inversion, and after returning to supine position (all P < .001). The post-inversion HR was less than pre-inversion (P = .03) and 3-min inversion HR (P = .003). There were significant changes in ICA and MCA flow caused by inversion, which affected blood flow velocity, resistance, and pulsatility index (all P ≤ .005). ConclusionInversion caused significant changes in ICP and blood flow. Thus, increased chance of complications may exist when using inversion as a therapeutic tool or during surgical procedures in patients with previous history of elevated ICP. These results demonstrate that inversion therapy should be used with caution.

Headstand (Sirshasana) Does Not Increase the Blood Flow to the Brain.

Objectives: Most yoga practitioners believe that headstand (Sirshasana) results in increased cerebral perfusion. This, however, is not consistent with autoregulation of the cerebral blood flow. The intent of this study was to demonstrate the effect of Sirshasana on the blood flow to the brain through ultrasound examination of the internal carotid artery (ICA). Design, location, and subjects: The ICA blood flow was measured with pulsed Doppler in 20 men and women aged 10 to 59 years (median 43) while performing the headstand (Sirshasana). Seventeen subjects were studied in 2018 in Spain at the altitude of 2,000 m, whereas the other three females were studied at sea level. Results: Although the diameter of the artery under examination during the headstand remained almost unchanged, the decrease in peak flow velocities in systole and diastole caused a significant decrease in arterial blood flow to the brain, followed by return to baseline values immediately after the antiorthostatic postural effect, likely due to the expected consequences of the cerebral blood flow autoregulation of the cerebral blood supply as well as the intracranial pressure. Conclusions: Contrary to popular belief, Sirshasana does not increase blood flow to the brain through the ICA, but results in predictable reduction in cerebral blood delivery in compliance with known mechanisms of autoregulation of cerebral blood flow. Moreover, increased ICA blood flow while performing the headstand is likely to be a contraindication to this exercise.

Four-Dimensional Flow MRI Analysis of Cerebral Blood Flow Before and After High-Flow Extracranial–Intracranial Bypass Surgery With Internal Carotid Artery Ligation

The hemodynamic changes that occur after high-flow (extracranial-intracranial) EC-IC bypass surgery with internal carotid artery (ICA) ligation are not well known. To assess blood flow changes after high-flow EC-IC bypass with ICA ligation by time-resolved 3-dimensional phase-contrast (4D Flow) magnetic resonance imaging (MRI). We enrolled 11 patients who underwent high-flow EC-IC bypass. 4D Flow MRI was performed before and after surgery to quantify the blood flow volume (BFV) of the ipsilateral ICA (BFViICA), bypass artery (BFVbypass), contralateral ICA (BFVcICA), and basilar artery (BFVBA). Subsequently, we calculated the total BFV (BFVtotal=BFViICA+BFVcICA+BFVBA [before surgery], BFVcICA+BFVBA+BFVbypass [after surgery]). The BFV changes after bypass was statistically analyzed. BFVbypass was slightly lower than BFViICA, but the difference was not statistically significant (3.84±0.94 vs 4.42±1.38 mL/s). The BFVcICA and BFVBA significantly increased after bypass surgery (BFVcICA 5.89±1.44 vs 7.22±1.37 mL/s [P=.0018], BFVBA 3.06±0.41 vs 4.12±0.38 mL/s [P<.001]). The BFVtotal significantly increased after surgery (13.37±2.58 vs 15.18±1.77 mL/s [P=.015]). There was no evidence of hyperperfusion syndrome in any cases. After high-flow EC-IC bypass with permanent ICA ligation, the bypass artery could partially compensate for the loss of BFV of the sacrificed ICA. The increased flow of the contralateral ICA and BA supply collateral blood flow. Clinically irrelevant hyperperfusion was observed.

Respiratory Variation of Internal Carotid Artery Blood Flow Peak Velocity Measured by Transfontanelle Ultrasound to Predict Fluid Responsiveness in Infants: A Prospective Observational Study.

Cranial sonography is a widely used point-of-care modality in infants. The authors evaluated that the respiratory variation of the internal carotid artery blood flow peak velocity as measured using transfontanelle ultrasound can predict fluid responsiveness in infants. This prospective observational study included 30 infants undergoing cardiac surgery. Following closure of the sternum, before and after the administration of 10ml · kg crystalloid, the respiratory variation of the aorta blood flow peak velocity, pulse pressure variation, and central venous pressure were obtained. The respiratory variation of the internal carotid artery blood flow peak velocity was measured using transfontanelle ultrasound. Response to fluid administration was defined as an increase in stroke volume index, as measured with transesophageal echocardiography, greater than 15% of baseline. Seventeen subjects (57%) were responders to volume expansion. Before fluid loading, the respiratory variation of the internal carotid artery and the aorta blood flow peak velocity (means ± SD) of the responders were 12.6 ± 3.3% and 16.0 ± 3.8%, and those of the nonresponders were 8.2 ± 3.2% and 10.9 ± 3.5%, respectively. Receiver operating characteristic curve analysis showed that the respiratory variation of the internal carotid artery and the aorta blood flow peak velocity could predict fluid responsiveness; the area under the curve was 0.828 (P < 0.0001; 95% CI, 0.647 to 0.940) and 0.86 (P = 0.0001; 95% CI, 0.684 to 0.959), respectively. The cutoff values of the respiratory variation of the internal carotid artery and the aorta blood flow peak velocity were 7.8% (sensitivity, 94%; specificity, 69%) and 13% (sensitivity, 77%; specificity, 92%), respectively. The respiratory variation of the internal carotid artery blood flow peak velocity as measured using transfontanelle ultrasound predicted an increase in stroke volume in response to fluid. Further research is required to establish any wider generalizability of the results.

The age‐related reduction in cerebral blood flow affects vertebral artery more than internal carotid artery blood flow

Ageing reduces cerebral blood flow (CBF), while mean arterial pressure (MAP) becomes elevated. According to 'the selfish brain' hypothesis of hypertension, a reduction in vertebral artery blood flow (VA) leads to increased sympathetic activity and thus increases MAP. In twenty-two young (24±3years; mean±SD) and eleven elderly (70±5years) normotensive men, duplex ultrasound evaluated whether the age-related reduction in CBF affects VA more than internal carotid artery (ICA) blood flow. Pulse-contour analysis evaluated MAP while near-infrared spectroscopy determined frontal lobe oxygenation and transcranial Doppler middle cerebral artery mean blood velocity (MCA Vmean ). During supine rest, MAP (90±13 versus 78±9mmHg; P<0·001) was elevated in the older subjects while their frontal lobe oxygenation (68±7% versus 77±7%; P<0·001), MCA Vmean (49±9 versus 60±12cm s-1 ; P=0·016) and CBF (754±112 versus 900±144mlmin-1 ; P=0·004) were low reflected in VA (138±48 versus 219±50mlmin-1 ; P<0·001) rather than in ICA flow (616±96 versus 680±120mlmin-1 ; P=0·099). In conclusion, blood supply to the brain and its oxygenation are affected by ageing and the age-related decline in VA flow appears to be four times as large as that in ICA and could be important for the age-related increase in MAP.