Cerebral Blood Flow Autoregulation Research Articles

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

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. 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. 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). 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.

Time-domain methods for quantifying dynamic cerebral blood flow autoregulation: Review and recommendations. A white paper from the Cerebrovascular Research Network (CARNet).

Cerebral Autoregulation (CA) is an important physiological mechanism stabilizing cerebral blood flow (CBF) in response to changes in cerebral perfusion pressure (CPP). By maintaining an adequate, relatively constant supply of blood flow, CA plays a critical role in brain function. Quantifying CA under different physiological and pathological states is crucial for understanding its implications. This knowledge may serve as a foundation for informed clinical decision-making, particularly in cases where CA may become impaired. The quantification of CA functionality typically involves constructing models that capture the relationship between CPP (or arterial blood pressure) and experimental measures of CBF. Besides describing normal CA function, these models provide a means to detect possible deviations from the latter. In this context, a recent white paper from the Cerebrovascular Research Network focused on Transfer Function Analysis (TFA), which obtains frequency domain estimates of dynamic CA. In the present paper, we consider the use of time-domain techniques as an alternative approach. Due to their increased flexibility, time-domain methods enable the mitigation of measurement/physiological noise and the incorporation of nonlinearities and time variations in CA dynamics. Here, we provide practical recommendations and guidelines to support researchers and clinicians in effectively utilizing these techniques to study CA.

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.

The impact of collateral therapeutics on stroke hemodynamics in normotensive and hypertensive rats: a step toward translation.

Stroke interventions that increase collateral flow have the potential to salvage penumbral tissue and increase the number of patients eligible for reperfusion therapy. We compared the efficacy of two different collateral therapeutics during transient middle cerebral artery occlusion (tMCAO) in normotensive and hypertensive rats. The change in collateral and core perfusion was measured using dual laser Doppler in response to either a pressor agent (phenylephrine, 10 mg/kg iv or vehicle) or a collateral vasodilator (TM5441, 5 mg/kg iv or vehicle) given 30 min into tMCAO in male Wistar and spontaneously hypertensive rats (SHRs). Pressor therapy increased collateral flow in the Wistar rats but was ineffective in the SHRs. The increase in collateral flow in the Wistar rats was associated with impaired cerebral blood flow autoregulation (CBFAR) that was intact in the SHRs. TM5441 caused a decrease in collateral perfusion in the Wistar rats and a modest increase in the SHRs. The pressor therapy reduced early infarction in both groups but increased edema in the SHRs, whereas TM5441 did not have any beneficial effects in either group. Thus, the pressor therapy was superior to a collateral vasodilator in increasing collateral flow and improving outcomes in the Wistar rats, likely due to pial collaterals that were pressure passive; the lack of CBF response in the SHRs to pressor therapy was likely due to intact CBFAR that limited perfusion. While TM5441 modestly increased CBF in the SHRs but not in the Wistar rats, it did not have a beneficial effect on stroke outcomes. These results suggest that collateral therapies may need to be selected for certain comorbidities.

Evaluation of the effect of intraventricular haemorrhage on cerebral perfusion in preterm neonates using three-dimensional pseudo-continuous arterial spin labelling.

Intraventricular haemorrhage (IVH) often arises as a cerebral complication directly related to preterm birth. The impaired autoregulation of cerebral blood flow is closely associated with IVH in preterm neonates. Three-dimensional pseudo-continuous arterial spin labelling (3D-pCASL) is a noninvasive magnetic resonance imaging (MRI) technique used for evaluating cerebral perfusion. This study aimed to compare cerebral blood flow values among three distinct groups using 3D-pCASL: preterm neonates with and without IVH and preterm neonates at term-equivalent age. A total of 101 preterm neonates who underwent conventional MRI and 3D-pCASL were included in this study. These neonates were categorised into three groups: 12 preterm neonates with IVH, 52 preterm neonates without IVH, and 37 healthy neonates at term-equivalent age. Cerebral blood flow measurements were obtained from six brain regions of interest (ROIs)-the frontal lobe, temporal lobe, parietal lobe, occipital lobe, basal ganglia, and thalamus-in the right and left hemispheres. The cerebral blood flow values measured in all ROIs of preterm neonates with IVH were significantly lower than those of neonates at term-equivalent age (all P<0.05). Additionally, the cerebral blood flow in the temporal lobe was lower in preterm neonates without IVH than in neonates at term-equivalent age (16.87±5.01 vs. 19.76±5.47 ml/100 g/min, P=0.012). Furthermore, a noteworthy positive correlation was observed between post-menstrual age and cerebral blood flow in the temporal lobe (P=0.037), basal ganglia (P=0.010), and thalamus (P=0.010). The quantitative cerebral blood flow values, as measured by 3D-pCASL, highlighted that preterm neonates with IVH had decreased cerebral perfusion. This finding underscores the potential of 3D-pCASL as a technique for evaluating the developmental aspects of the brain in preterm neonates.

The Role of Nitric Oxide in the Autoregulation of Cerebral Blood Flow and the Pathogenesis of Cerebral Vascular Spasm in Patients with Ruptured Cerebral Aneurysms

The presented literature review is devoted to the role of the endothelial relaxing factor – nitric oxide (NO) – in the regulation of cerebral blood flow in patients with ruptured intracranial aneurysms. Modern views on the physiology of NO, methods of regulation and autoregulation of its synthesis are described, experimental and clinical data on the disruption of the production of the endothelial relaxing factor in subarachnoid hemorrhage are presented.

Rheoencephalography: A non-invasive method for neuromonitoring.

In neurocritical care, the gold standard method is intracranial pressure (ICP) monitoring for the patient's lifesaving. Since it is an invasive method, it is desirable to use an alternative, noninvasive technique. The computerized real-time invasive cerebral blood flow (CBF) autoregulation (AR) monitoring calculates the status of CBF AR, called the pressure reactivity index (PRx). Studies documented that the electrical impedance of the head (Rheoencephalography - REG) can detect the status of CBF AR (REGx) and ICP noninvasively. We aimed to test REG to reflect ICP and CBF AR. For nineteen healthy subjects we recorded bipolar bifrontal and bitemporal REG derivations and arm bioimpedance pulses with a 200 Hz sampling rate. The challenges were a 30-second breath-holding and head-down-tilt (HDT - Trendelenburg) position. Data were stored and processed offline. REG pulse wave morphology and REGx were calculated. The most relevant finding was the significant morphological change of the REG pulse waveform (2nd peak increase) during the HDT position. Breath-holding caused REG amplitude increase, but it was not significant. REGx in male and female group averages have similar trends during HDT by indicating the active status of CBF AR. The morphological change of REG pulse wave during HDT position was identical to ICP waveform change during increased ICP, reflecting decreased intracranial compliance. A correlation study between ICP and REG was initiated in neurocritical care patients. The noninvasive REG monitoring would also be useful in space research as well as in military medicine during the transport of wounded service members as well as for fighter pilots to indicate the loss of CBF and consciousness.

Our initial experience of monitoring the autoregulation of cerebral blood flow during cardiopulmonary bypass

Background: Cerebral blood flow (CBF) is believed to be relatively constant within an upper and lower blood pressure limit. Different methods are available to monitor CBF autoregulation during surgery. This study aims to critically analyze the application of the cerebral oxygenation index (COx), one of the commonly used techniques, using a reference to data from a series of clinical registrations. Method: CBF was monitored using near-infrared spectroscopy, while cerebral blood pressure was estimated by recordings obtained from either the radial or femoral artery in 10 patients undergoing cardiopulmonary bypass. The association between CBF and blood pressure was calculated as a moving continuous correlation coefficient. A COx index &gt; 0.4 was regarded as a sign of abnormal cerebral autoregulation (CA). Recordings were examined to discuss reliability measures and clinical feasibility of the measurements, followed by interpretation of individual results, identification of possible pitfalls, and suggestions of alternative methods. Results and Conclusion: Monitoring of CA during cardiopulmonary bypass is intriguing and complex. A series of challenges and limitations should be considered before introducing this method into clinical practice.

Impaired intracellular Ca2+ signaling contributes to age-related cerebral small vessel disease in Col4a1 mutant mice.

Humans and mice with mutations in COL4A1 and COL4A2 manifest hallmarks of cerebral small vessel disease (cSVD). Mice with a missense mutation in Col4a1 at amino acid 1344 (Col4a1+/G1344D) exhibit age-dependent intracerebral hemorrhages (ICHs) and brain lesions. Here, we report that this pathology was associated with the loss of myogenic vasoconstriction, an intrinsic vascular response essential for the autoregulation of cerebral blood flow. Electrophysiological analyses showed that the loss of myogenic constriction resulted from blunted pressure-induced smooth muscle cell (SMC) membrane depolarization. Furthermore, we found that dysregulation of membrane potential was associated with impaired Ca2+-dependent activation of large-conductance Ca2+-activated K+ (BK) and transient receptor potential melastatin 4 (TRPM4) cation channels linked to disruptions in sarcoplasmic reticulum (SR) Ca2+ signaling. Col4a1 mutations impair protein folding, which can cause SR stress. Treating Col4a1+/G1344D mice with 4-phenylbutyrate, a compound that promotes the trafficking of misfolded proteins and alleviates SR stress, restored SR Ca2+ signaling, maintained BK and TRPM4 channel activity, prevented loss of myogenic tone, and reduced ICHs. We conclude that alterations in SR Ca2+ handling that impair ion channel activity result in dysregulation of SMC membrane potential and loss of myogenic tone and contribute to age-related cSVD in Col4a1+/G1344D mice.

Blood pressure-cerebral oxygen coupling model: A new approach for stroke risk prediction.

Stroke is a major cause of death and disability worldwide, but predicting its risk remains challenging. This study aimed to evaluate the cerebral blood flow autoregulation function of subjects with different stroke risk levels and predict their stroke risk. The coupling strength between cerebral oxygen and blood pressure signals was calculated by wavelet analysis and dynamic Bayesian inference and used as a quantitative index of cerebral blood flow autoregulation. A stroke prediction model based on the extreme random tree was constructed using the coupling strength and other data as input features. The results showed that the coupling strength was significantly higher in the high-risk group than the other groups. Moreover, the prediction model achieved an average accuracy of 0.80 across the three groups. The coupling strength of cerebral oxygen and blood pressure can be used as an objective index to predict stroke risk, which has implications for stroke prevention and intervention.

Autoregulation of cerebral blood flow in normal and pathological conditions

The metabolic needs of the brain largely depend on the intensity of the functioning of its various departments, which requires constant regulation of the level of local blood flow. The importance of accurate and timely regulation of cerebral blood flow is enhanced by the lack of substrate stores for autonomous energy production in nervous tissue. In this case, the state of systemic hemodynamics can have a significant effect on organ blood flow. At the same time, given the significant importance of the central nervous system in providing all physiological processes, the regulation of organ cerebral blood flow is aimed at minimizing the possible adverse consequences of the influence of disorders of systemic hemodynamics. In this regard, the regulation of cerebral blood flow is based on multiple and complex physiological mechanisms at various levels. The basic level of regulation of cerebral blood flow is myogenic response, which provides the phenomenon of autoregulation of blood flow in the brain. The review focuses on the physiological mechanisms underlying myogenic regulation as well as the change in this regulation in various diseases.

Abstract 15140: Cerebral Hemodynamics During Left Ventricular Assist Device Speed Titration

Introduction: Left ventricular assist device (LVAD) speed may be titrated to optimize cardiopulmonary hemodynamics, but the impact on cerebral blood flow remains poorly understood. Hypothesis: Here, we monitored cerebral hemodynamics during ramp studies, to test the hypothesis that LVAD speed correlates with cerebral blood flow and cerebral autoregulation. Methods: Patients with HeartMate3 LVADs underwent ramp study for optimization, during which cerebral blood flow velocity (CBFv) was continuously monitored by transcranial Doppler (TCD), and blood pressure was continuously monitored by finger plethysmography. Mx index was used a measure of autoregulation which correlates blood pressure and CBFv (i.e. high Mx index indicates poor autoregulation). The treating cardiologist determined the optimal speed based on cardiopulmonary dynamics (other speeds were categorized as sub-optimal). Results: Of 23 patients, 5 did not undergo speed changes. At least two speeds were explored in the remaining 18 patients. When comparing the lowest and highest speeds for each patient, higher speeds resulted in higher CBFv (p=0.02; Figure 1a ), but no change in autoregulation (p=0.38; Figure 1b ). However, when comparing the optimal and suboptimal LVAD speeds, CVFv was similar (p=0.89; Figure 2a ,), whereas the optimal speed was associated with a trend toward favorable autoregulation (p=0.09; Figure 2b ). Conclusions: Cerebral blood flow velocity is sensitive to LVAD speed titration, and cardiopulmonary optimization may improve cerebral autoregulation. A larger cohort and a broader range of speeds may further clarify the impact of speed titration on cerebral hemodynamics.

Intraoperative Anesthetic Management of Bilateral Intraventricular Hemorrhage Secondary to Anterior Communicating Artery Aneurysm Rupture in Hypertensive Patient

Introduction: Primary (IVH) is non traumatic intracerebral hemorrhage confined to the ventricular system which is relatively infrequent, but is more commonly caused by hypertensive (52%) hemorrhagic stroke, followed by trauma (15%), intraventricular arteriovenous malformation (7.5%), coagulopathy (7.5%), diabetic vasculopathy (7.5%), anterior communicating artery aneurysms (3%), and undetectable cause. Clipping of ruptured anterior communicating artery with hypertension possess anesthetic challenges in managing intra-operatively, and when it comes for an ideal neuroprotective agent, barbiturates induced anesthesia was planned. Case Report: A 70 years old male came to our hospital with history of sudden loss of consciousness and a known case of systemic hypertension for 3 years and was on irregular medications, intubated in emergency medicine department in view of low GCS which was difficult intubation. CT brain Angiogram was done and diagnosed as ruptured Anterior Communicating Artery Aneurysm and underwent Aneurysmal clipping of anterior communicating artery aneurysm under general anesthesia. Emergency medications were kept ready. Intensive neuro monitoring, invasive blood pressure monitoring and to decrease the intraoperative intracranial pressure, to preserve autoregulation of cerebral blood flow, barbiturates induced anesthesia were planned (thiopentone as an induction agent and maintained with inhalational anesthetic agent). Patient was shifted to ICU for observation and extubated on next day uneventfully. Conclusion: We present a successful anesthetic management of hypertensive patient with ruptured anterior communicating artery who underwent clipping of aneurysm. A detailed pre-anesthetic evaluation and proper planning is utmost important to encounter the risk of ischemic injury to brain while clipping of ruptured aneurysmal vessel.

Additional predictors of the lower limit of cerebral autoregulation during cardiac surgery.

The lower limit of autoregulation (LLA) of cerebral blood flow was previously shown to vary directly with the Ambulatory Arterial Stiffness Index (AASI) redefined as 1-regression slope of DBP-versus-SBP readings invasively measured from the radial artery before the bypass. We aimed expanding the predictive capacity of the LLA with AASI by combining it with additional predictors and provide new indications whether mean arterial pressure (MAP) is above/below the LLA. In 181 patients undergoing cardiac surgery, mean (SD) age 71 (8) years), we identified from the demographic, preoperative and intraoperative characteristics independent and statistically significant 'single predictors' of the LLA (including AASI). This was achieved using multivariate linear regression with a backward-elimination technique. The single predictors combined with 1-AASI generated new multiplicative and additive composite predictors of the LLA. Indicators for the MAP-to-LLA difference (DIF) were determined using DIF-versus-predictor plots. The odds ratio (OR) for the DIF sign (Outcome = 1 for DIF≤0) and predictor-minus-median sign (Exposure = 1 for Predictor ≤ Median) were calculated using logistic regression. BMI, 1-AASI and systolic coefficient of variation were identified single predictors that correlated similarly with the LLA ( r = -0.26 to -0.27, P < 0.001). The multiplicative and additive composite predictors displayed higher correlation with LLA ( r = -0.41 and r = -0.43, respectively, P < 0.001) and improved LLA estimation. The adjusted OR for the composite predictors was nearly twice that of the single predictors. The novel composite predictors may enhance the LLA estimation and the ability to maintain MAP in the cerebral autoregulatory range during cardiac surgery.

Abstract 062: Lower Middle Cerebral Artery Resistance In A Transgenic Rat Model Of Preeclampsia: A Platform For Studying Long-term Preeclampsia Induced Cerebrovascular Disease

Preeclampsia (PE) is a pregnancy disorder characterized by new onset hypertension and end-organ dysfunction. PE patients have increased risk of cerebrovascular disease (CVD) later in life; however, the mechanisms are unclear. We determined whether exposure to a PE-like syndrome in transgenic rat (TGA-PE: female TG for angiotensinogen mated to male TG for renin) alters left middle cerebral artery (LMCA) or left internal carotid (LICA) artery hemodynamics at 2 or 5 months post-pregnancy. The analyses of systolic (SBP) and diastolic (DBP) blood pressures and heart rate (HR) (by tail cuff; NIBP-8 Columbus Instruments), and LMCA and LICA pulsatility index (PI) (by transcranial Doppler (TCD); Vevo 2100), were performed at late gestation, and at 2 and 5 months post-pregnancy. SBP and DBP were elevated in TGA-PE vs. Sprague-Dawley (SD) in late pregnancy (n=5-6), and at 2 (n=4-6), and 5 months (n=2-3) post-pregnancy (p&lt;0.05). HR was elevated in TGA-PE vs. SD in late pregnancy (493.5±10.6 vs. 392.5±14.2, p&lt;0.05, n=5-6), but not at 2 or 5 months post-pregnancy. However, LMCA PI was lower in TGA-PE vs. SD at 2 months post-pregnancy (p&lt;0.05), and tended to decrease in late gestation and at 5 months post-pregnancy. LICA PI was lower in TGA-PE vs. SD during pregnancy (0.729 ± 0.086 vs 1.34 ± 0.095, p&lt;0.05, n=4-5). In summary, PE-like syndrome in TGA-PE resulted in higher SBP and lower LMCA resistance versus SD at 2 months post-pregnancy, suggesting a dysfunctional autoregulation of cerebral blood flow. Since women with history of PE have lower MCA resistance, we conclude that TGA-PE model may provide a suitable platform to investigate the mechanistic link between PE and future development of CVD.

Abstract P422: CD4+ T Cells From Preeclamptic Patients During Pregnancy Causes Cognitive Dysfunction Postpartum In A Pregnant Rat Model

Preeclampsia (PE), new onset hypertension (HTN) during pregnancy, is associated with impaired cognitive function and increased cerebral blood flow (CBF). Although we have previously shown adoptive transfer of placental CD4+ T cells from PE women into athymic nude pregnant rats causes HTN and circulating factors associated with PE, we do not know the role of CD4+ T cells in contributing to impaired cerebral blood flow and cognitive dysfunction in the postpartum period. Therefore, we hypothesize that adoptive transfer of placental CD4+ T cells from PE patients into pregnant athymic nude recipient rats will cause maternal hypertension and cognitive dysfunction and impaired CBF postpartum. Placental CD4+ T cells were isolated from normotensive (NP) and preeclamptic (PE) pregnant women at delivery. One million CD4+ T cells were injected interperitoneally (i.p.) into normal pregnant nude athymic rats on gestational day (GD) 12. Dams were allowed to deliver and aged 12-weeks after delivery. Blood pressure (MAP) was measured by carotid catheter and at 12-weeks postpartum CBF autoregulation was measured by laser Doppler flowmetry. The Barnes maze and the novel object recognition behavioral assays were used to assess cognitive function on gestational day (GD) 15-19 and 12-weeks postpartum. A student’s t-test was used for statistical analysis. MAP increased during pregnancy in PE recipient rats (115±2 mmHg, n=5) compared to NP recipient rats (99±3 mmHg, n=4, p&lt; 0.05). MAP significantly increased in the postpartum period in PE recipient rats (114±2 mmHg, n=5) compared to NP controls (98±2 mmHg, n=7, p&lt;0.05). PE recipient rats exhibited latency with errors navigating in the Barnes maze compared to NP controls during pregnancy and postpartum. Locomotor activity was decreased in PE recipient rats compared to NP controls during pregnancy (p&lt;0.05) and postpartum. PE recipient rats had increased CBF autoregulation compared to NP rat recipients in the postpartum period. Our findings indicate that rat recipients of CD4+ T cells from PE patients demonstrate maternal HTN and increased CBF and cognitive dysfunction in the postpartum period compared to recipients of NP CD4 + T cells. These data indicate long-term cognitive and cerebral dysfunction as a result of preeclampsia.

Assessment of cerebral autoregulatory function and inter-hemispheric blood flow in older adults with internal carotid artery stenosis using transcranial Doppler sonography-based measurement of transient hyperemic response after carotid artery compression

Unhealthy vascular aging promotes atherogenesis, which may lead to significant internal carotid artery stenosis (CAS) in 5 to 7.5% of older adults. The pathogenic factors that promote accelerated vascular aging and CAS also affect the downstream portion of the cerebral microcirculation in these patients. Primary treatments of significant CAS are eversion endarterectomy or endarterectomy with patch plasty. Factors that determine adequate hemodynamic compensation and thereby the clinical consequences of CAS as well as medical and surgical complications of carotid reconstruction surgery likely involve the anatomy of the circle of Willis (CoW), the magnitude of compensatory inter-hemispheric blood flow, and the effectiveness of cerebral microcirculatory blood flow autoregulation. This study aimed to test two hypotheses based on this theory. First, we hypothesized that patients with symptomatic and asymptomatic CAS would exhibit differences in autoregulatory function and inter-hemispheric blood flow. Second, we predicted that anatomically compromised CoW would associate with impaired inter-hemispheric blood flow compensation. We enrolled older adults with symptomatic or asymptomatic internal CAS (>70% NASCET criteria; n = 46) and assessed CoW integrity by CT angiography. We evaluated transient hyperemic responses in the middle cerebral arteries (MCA) after common carotid artery compression (CCC; 10 s) by transcranial Doppler sonography (TCD). We compared parameters reflecting autoregulatory function (e.g., transient hyperemic response ratio [THRR], return to baseline time [RTB], changes of vascular resistance) and inter-hemispheric blood flow (residual blood flow velocity). Our findings revealed that CAS was associated with impaired cerebral vascular reactivity. However, we did not observe significant differences in autoregulatory function or inter-hemispheric blood flow between patients with symptomatic and asymptomatic CAS. Moreover, anatomically compromised CoW did not significantly affect these parameters. Notably, we observed an inverse correlation between RTB and THRR, and 49% of CAS patients exhibited a delayed THRR, which associated with decreased inter-hemispheric blood flow. Future studies should investigate how TCD-based evaluation of autoregulatory function and inter-hemispheric blood flow can be used to optimize surgical techniques and patient selection for internal carotid artery revascularization.

AT1-AA Infusion during Pregnancy Impairs CBF Autoregulation Postpartum.

Preeclampsia (PE), new-onset hypertension during pregnancy alongside organ dysfunction, is a leading cause of morbidity and mortality for the mother and fetus. PE women have activated B cells that produce agonistic autoantibodies to the angiotensin II type 1 receptor (AT1-AA). AT1-AA impairs cerebral blood flow (CBF) autoregulation during pregnancy. Although AT1-AA often remains elevated up to 8 years postpartum, AT1-AA's effect on CBF autoregulation postpartum is unknown. This study examined whether elevated AT1-AA during pregnancy impairs CBF autoregulation postpartum and if this was augmented by infusion of AT1-AA postpartum. AT1-AA was infused into 12-week-old timed-pregnant Sprague Dawley rats beginning on gestational day 14. Uterine artery resistance index (UARI) was measured on gestational day 18 as a measure of endothelial dysfunction associated with PE. Dams were allowed to deliver. One group was given a second infusion of AT1-AA (50% perinatal dose mimicking levels observed in postpartum PE women) at 9 weeks postpartum. After postpartum week 10, mean arterial pressure (MAP) was measured in conscious rats and CBF autoregulation was measured by laser Doppler flowmetry. AT1-AA during pregnancy increased UARI (P<0.05). AT1-AA during pregnancy did not affect MAP postpartum but did impair CBF autoregulation postpartum. Infusion of AT1-AA postpartum significantly elevated blood pressure (P<0.01) but did not further impair CBF autoregulation. This study demonstrates that circulating AT1-AA during pregnancy causes impairment of CBF autoregulation well into the postpartum period indicating that elevated AT1-AA leads to long-term cerebrovascular consequences. Targeting AT1-AA may prevent cerebrovascular effects associated with PE during pregnancy and postpartum.

Estimating Hemodynamic Significant Deformations of Brachiocephalic Arteries Using CT Perfusion

Background and Aim: The cause of most strokes is associated with the pathology of the carotid arteries. Many modern researchers suggest preventive surgery in the presence of arterial deformity to prevent strokes. The hemodynamic significance of carotid deformities is determined by morphological and functional disorders at the level of tortuosity, the reaction of cerebral blood flow is not often considered. Here, we assume that cerebral autoregulation in tortuosity can be different. Methods and Materials/Patients: A total of 64 patients (31-75 years old) with 110 carotid deformities were analyzed. Duplex color mapping, computed tomography angiography of carotid arteries, and computed tomography perfusion were performed by estimating the absolute and average values of cerebral blood flow (mL/100 g/min), cerebral blood volume (mL/100 g), Mean transit time (MTT) (s) in similar areas of the cortex. In 6 patients, the acetazolamide challenge test was used to evaluate the autoregulatory disturbances. Results: According to computed tomography angiography and duplex color mapping, 18(28.1%) patients had unilateral tortuosity, and 46(71.9%) patients had bilateral tortuo s ity. Hemodynamically significant deformities were detected in 33 cases (30% of tortuosity). In 54 cases (49% of tortuosity), the deformities were accompanied by carotid stenosis. Perfusion disorders were detected in 23 of 64 patients (35.9%). In the majority of cases (75% of all perfusion disorders), hypoperfusion was diagnosed on the side corresponding to the maximum degree of stenosis, regardless of the location of the tortuosity. Neurologically significant hypoperfusion, compensated by collateral blood flow revealed only in 7.8% of cases of hemodynamic significant internal carotid artery deformity without concomitant atherosclerosis. Conclusion: The decision on surgical correction of carotid artery tortuosity should be made while considering both local changes in hemodynamics and proven violations of autoregulation of cerebral blood flow, especially in patients with concomitant carotid stenosis.

Cerebral blood flow autoregulation assessment by correlation analysis between mean arterial blood pressure and transcranial doppler sonography or near infrared spectroscopy is different: A pilot study.

Recently, cerebral autoregulation indices based on moving correlation indices between mean arterial pressure (MAP) and cerebral oximetry (NIRS, ORx) or transcranial Doppler (TCD)-derived middle cerebral artery flow velocity (Mx) have been introduced to clinical practice. In a pilot study, we aimed to evaluate the validity of these indices using incremental lower body negative pressure (LBNP) until presyncope representing beginning cerebral hypoperfusion as well as lower body positive pressure (LBPP) with added mild hypoxia to induce cerebral hyperperfusion in healthy subjects. Five male subjects received continuous hemodynamic, TCD and NIRS monitoring. Decreasing levels of LBNP were applied in 5-minute steps until subjects reached presyncope. Increasing levels of LBPP were applied stepwise up to 20 or 25 mmHg. Normobaric hypoxia was added until an oxygen saturation of 84% was reached. This was continued for 10 minutes. ORx and Mx indices were calculated using previously described methods. Both Indices showed an increase > 0.3 indicating impaired cerebral autoregulation during presyncope. However, there was no significant difference in Mx at presyncope compared to baseline (p = 0.168). Mean arterial pressure and cardiac output decreased only in presyncope, while stroke volume was decreased at the last pressure level. Neither Mx nor ORx showed significant changes during LBPP or hypoxia. Agreement between Mx and ORx was poor during the LBNP and LBPP experiments (R2 = 0.001, p = 0.3339). Mx and ORx represent impaired cerebral autoregulation, but in Mx this may not be distinguished sufficiently from baseline. LBPP and hypoxia are insufficient to reach the upper limit of cerebral autoregulation as indicated by Mx and ORx.