脑梗死早期血流动力学模型的研究

脑梗死发病早期，血管闭塞直接造成了脑血流动力学的变化．为定量研究梗死发生后缺血脑组织残余血流变化和多种变量间的关系，本文使用血流动力学的相关原理，依据脑血流自动调节机制，在理论上建立影响残余血流的数学模型，并结合临床对该模型进行讨论和研究．     

Hemodynamic Effect of Cerebral Vasospasm in Humans: A Modeling Study

A mathematical model of cerebral hemodynamics during vasospasm is presented. The model divides arterial hemodynamics into two cerebral territories: with and without spasm. It also includes collateral circulation between the two territories, cerebral venous hemodynamics, cerebrospinal fluid circulation, intracranial pressure (ICP) and the craniospinal storage capacity. Moreover, the pial artery circulation in both territories is affected by cerebral blood flow (CBF) autoregulation mechanisms. In this work, a numerical value to model parameters was given assuming that vasospasm affects only a single middle cerebral artery (MCA). In a first stage, the model is used to simulate some clinical results reported in the literature, concerning the patterns of MCA velocity, CBF and pressure losses during vasospasm. The agreement with clinical data turns out fairly good. In a second stage, a sensitivity analysis on some model parameters is performed (severity of caliber reduction, longitudinal extension of the spasm, autoregulation gain, ICP, resistance of the collateral circulation, and mean systemic arterial pressure) to clarify their influence on hemodynamics in the spastic territory. The results suggest that the clinical impact of vasospasm depends on several concomitant factors, which should be simultaneously taken into account to reach a proper diagnosis. In particular, while a negative correlation between MCA velocity and cross sectional area can be found until CBF is well preserved, a positive correlation may occur when CBF starts to decrease significantly. This might induce false-negative results if vasospasm is assessed merely through velocity measurements performed by the transcranial Doppler technique. © 1999 Biomedical Engineering Society. PAC99: 8719Uv, 8719La, 8710+e     

Regional,segmental, and temporal heterogeneity of cerebral vascular autoregulation

Autoregulation of cerebral blood flow is heterogeneous in several ways: regional, segmental, and temporal. We have found regional heterogeneity of the autoregulatory response during both acute reductions and increases in systemic arterial presure. Changes in blood flow are less in brain stem than in cerebrum during decreases and increases in cerebral perfusion pressure. Segmental heterogeneity of autoregulation has been demonstrated in two ways. Direct determination of segmental cerebral vascular resistance indicates that, while small cerebral vessels (<200 μm in diameter) make a major contribution to autoregulation during acute increases in pressure between 80 and 100 mm Hg, the role of large cerebral arteries (>200 μm) becomes increasingly important to the autoregulatory response at pressures above 100 mm Hg. Measurement of changes in diameter of pial vessels has shown that, during acute hypotension, autoregulation occurs predominantly in small resistance vessels (<100 μm). Finally, there is temporal heterogeneity of autoregulation. Sudden increases in arterial pressure produce transient increases in blood flow, which are not observed under steady-state conditions. In addition, the blood-brain barrier is more susceptible to hypertensive disruption after rapid, compared to step-wise, increases in arterial pressure. Thus, when investigating cerebral vascular autoregulation, regional, segmental, and temporal differences in the autoregulatory response must be taken into consideration.     

Closed-Loop Dynamic Modeling of Cerebral Hemodynamics

The dynamics of cerebral hemodynamics have been studied extensively because of their fundamental physiological and clinical importance. In particular, the dynamic processes of cerebral flow autoregulation (CFA) and CO₂ vasomotor reactivity have attracted broad attention because of their involvement in a host of pathologies and clinical conditions (e.g., hypertension, syncope, stroke, traumatic brain injury, vascular dementia, Alzheimer’s disease, mild cognitive impairment etc.). This raises the prospect of useful diagnostic methods being developed on the basis of quantitative models of cerebral hemodynamics, if cerebral vascular dysfunction can be quantified reliably from data collected within practical clinical constraints. This paper presents a modeling method that utilizes beat-to-beat measurements of mean arterial blood pressure, cerebral blood flow velocity and end-tidal CO₂ (collected non-invasively under resting conditions) to quantify the dynamics of CFA and cerebral vasomotor reactivity (CVMR). The unique and novel aspect of this dynamic model is that it is nonlinear and operates in a closed-loop configuration.     

A multinephron model of renal blood flow autoregulation by tubuloglomerular feedback and myogenic response

Tubuloglomerular feedback implies that a primary increase in arterial pressure, renal blood flow, glomerular filtration and increased flow rate in the distal tubule increase preglomerular resistance and thereby counteract the primary rise in glomerular filtration rate and renal blood flow. Tubuloglomerular feedback has therefore been assumed to play a role in renal autoregulation, i.e., the constancy of renal blood flow and glomerular filtration at varying arterial pressure. In evaluating this hypothesis, the numerous tubular and vascular mechanisms involved have called for mathematical models. Based on a single nephron model we have previously concluded that tubuloglomerular feedback can account for only a small part of blood flow autoregulation. We now present a more realistic multinephron model, consisting of one interlobular artery with an arbitrary number of evenly spaced afferent arterioles. Feedback from the distal tubule was simulated by letting glomerular blood flow exert a positive feedback on preglomerular resistance, in each case requiring compatibility with experimental open-loop responses in the most superficial nephron. The coupling together of 10 nephrons per se impairs autoregulation of renal blood flow compared to that of a single nephron model, but this effect is more than outweighed by greater control resistance in deep arterioles. Some further improvement was obtained by letting the contractile response spread from each afferent arteriole to the nearest interlobular artery segment. Even better autoregulation was provided by spreading of full strength contraction also to the nearest upstream or downstream afferent arteriole, and spread to both caused a renal blood flow autoregulation approaching experimental observations. However, when the spread effect was reduced to 25% of that in each stimulated afferent arteriole, more compatible with recent experimental observations, the autoregulation was greatly impaired. Some additional mechanism seems necessary, and we found that combined myogenic response in interlobular artery and tubuloglomerular feedback regulation of afferent arterioles can mimic experimental pressure-flow curves.     

Preserved dynamic cerebral autoregulation in the middle cerebral artery among persons with migraine

Migraine affects the autonomous nervous system and a recent investigation has also proposed a severe disturbance of dynamic cerebral blood flow regulation in the middle cerebral artery during spontaneous blood pressure oscillations. This study investigates whether dynamic cerebral autoregulation is impaired in persons with migraine among a normal cohort. Out of 94 adults studied to establish normal values for dynamic autoregulation, 19 suffered from migraine according to IHS criteria (10 of them with aura). Transcranial Doppler sonography and fingerplethysmography were used to determine dynamic autoregulation of both middle cerebral arteries following spontaneous low frequency (0.06–0.12 Hz) blood pressure fluctuations (phase and gain of transfer function, correlation coefficient indices Dx and Mx). No significant differences were found for the low frequency variability of blood pressure (power spectral density) and various indices of dynamic cerebral autoregulation between persons with and without migraine. Moreover, no differences were observed between persons with migraine, with and without aura. This study based on a normal cohort does not support the presence of generally impaired cerebral autoregulation dynamics in persons with migraine. Future studies should focus on posterior circulation and particular cerebellar autoregulation.     

Dynamic pressure–flow relationship of the cerebral circulation during acute increase in arterial pressure

The physiological mechanism(s) for the regulation of the dynamic pressure–flow relationship of the cerebral circulation are not well understood. We studied the effects of acute cerebral vasoconstriction on the transfer function between spontaneous changes in blood pressure (BP) and cerebral blood flow velocity (CBFV) in 13 healthy subjects (30 ± 7 years). CBFV was measured in the middle cerebral artery using transcranial Doppler. BP was increased stepwise with phenylephrine infusion at 0.5, 1.0 and 2.0 μg kg^–1 min^–1. Phenylephrine increased BP by 11, 23 and 37% from baseline, while CBFV increased (11%) only with the highest increase in BP. Cerebrovascular resistance index (BP/CBFV) increased progressively by 6, 17 and 23%, demonstrating effective steady-state autoregulation. Transfer function gain at the low frequencies (LF, 0.07–0.20 Hz) was reduced by 15, 14 and 14%, while the phase was reduced by 10, 17 and 31%. A similar trend of changes was observed at the high frequencies (HF, 0.20–0.35 Hz), but gain and phase remained unchanged at the very low frequencies (VLF, 0.02–0.07 Hz). Windkessel model simulation suggests that increases in steady-state cerebrovascular resistance and/or decreases in vascular compliance during cerebral vasoconstriction contribute to the changes in gain and phase. These findings suggest that changes in steady-state cerebrovascular resistance and/or vascular compliance modulate the dynamic pressure–flow relationship at the low and high frequencies, while dynamic autoregulation is likely to be dominant at the very low frequencies. Thus, oscillations in CBFV are modulated not only by dynamic autoregulation, but also by changes in steady-state cerebrovascular resistance and/or vascular compliance.     

The influence of an unilateral carotid artery stenosis on brain oxygenation

We study the impact of varying degrees of unilateral stenoses of an carotid artery on pulsatile blood flow and oxygen transport from the heart to the brain. For the numerical simulation a model reduction approach is used involving non-linear 1-D transport equation systems, linear 1-D transport equations and 0-D models. The haemodynamic effects of vessels beyond the outflow boundaries of the 1-D models are accounted for using a 0-D lumped three element windkessel model. At the cerebral outflow boundaries the 0-D windkessel model is extended by metabolic autoregulation, based on the cerebral oxygen supply. Additionally lumped parameter models are applied to incorporate the impact of the carotid stenosis. Our model suggests that for a severe unilateral stenosis in the right carotid artery the partial pressure of oxygen in the brain area at risk can only be restored, if the corresponding cerebral resistance is significantly decreased and if the circle of Willis (CoW) is complete.     

Effects of Autoregulation and CO<Subscript>2</Subscript> Reactivity on Cerebral Oxygen Transport

Both autoregulation and CO₂ reactivity are known to have significant effects on cerebral blood flow and thus on the transport of oxygen through the vasculature. In this paper, a previous model of the autoregulation of blood flow in the cerebral vasculature is expanded to include the dynamic behavior of oxygen transport through binding with hemoglobin. The model is used to predict the transfer functions for both oxyhemoglobin and deoxyhemoglobin in response to fluctuations in arterial blood pressure and arterial CO₂ concentration. It is shown that only six additional nondimensional groups are required in addition to the five that were previously found to characterize the cerebral blood flow response. A resonant frequency in the pressure-oxyhemoglobin transfer function is found to occur in the region of 0.1 Hz, which is a frequency of considerable physiological interest. The model predictions are compared with results from the published literature of phase angle at this frequency, showing that the effects of changes in breathing rate can significantly alter the inferred phase dynamics between blood pressure and hemoglobin. The question of whether dynamic cerebral autoregulation is affected under conditions of stenosis or stroke is then examined.     

Relationship between Myogenic Reaction and Autoregulation of Cerebral Circulation

Dilatation of rat pial arterioles at constant arteriolar wall strain during autoregulation of cerebral circulation was shown by the method of biomicroscopy. Wavelet-analysis of cerebral blood flow oscillations during this period revealed increased oscillation amplitude in the endothelial and neurogenic frequency ranges and unchanged amplitude at myogenic frequency range. These findings probably attest to the leading role of myogenic reaction in the autoregulation.     

Cerebral vasodilatation induced by stimulation of the pterygopalatine ganglion and greater petrosal nerve in anesthetized monkeys

Although brain cell viability depends largely on cerebral circulation, mechanisms of blood flow control, such as autoregulation, or of the pathogenesis of functionally impaired blood supply to brain regions, such as in cerebral vasospasm after subarachnoid hemorrhage, have not been clearly defined. Our recent studies support the hypothesis that nitric oxide, released from nitrergic nerves, plays a crucial role as a neurotransmitter in vasodilating cerebral arteries from primate and subprimate mammals. In the present study, we demonstrated, by using arterial angiography, that electrical stimulation of the pterygopalatine ganglion produced vasodilatation of ipsilateral cerebral arteries of anesthetized Japanese monkeys. The response was abolished by intravenous injections of N(G)-nitro-L-arginine, a nitric oxide synthase inhibitor. Denervation of the ganglion elicited cerebral vasoconstriction, indicating that vasodilator nerves from the vasomotor center were tonically active. Stimulation of the greater petrosal nerve, upstream of the pterygopalatine ganglion, also elicited cerebral vasodilatation, which was abolished by treatment with the nitric oxide synthase inhibitor and with hexamethonium, indicating that the nerve is in connection via synapses with the nitrergic nerve innervating cerebral arteries. Endogenous nitric oxide released from the nerve may contribute to the maintenance of blood flow in major cerebral arteries necessary to supply blood to the different brain regions. Without this influence, cerebral arteries might be constricted to the extent that blood flow is impeded.This is the first direct evidence indicating an important role of nitric oxide liberated by pre- and postganglionic nerve stimulation in the control of cerebral arterial tone in primates.     

小型幼猪体外循环模型灌注流量对脑血流灌注的影响

目的建立幼猪体外循环(cardiopulmonary bypass,CPB)模型,观察CPB灌注流量发生改变期间,脑灌注流量和局部脑氧饱和度(regional cerebral oxygen saturation,rSO_2)的变化,从而探索CPB灌注流量对脑血流量自我调节的影响,以期为婴幼儿CPB合理的灌注管理、预防脑缺血提供理论依据。方法 12只幼猪按照随机表分为3组,对照组、高流量组(H组)、低流量组(L组)。建立单泵双管CPB灌注模型,用血流检测仪直接检测灌注管路流量反映不同流量下脑动脉内血液灌注的变化,并采用近红外分光广度检测技术(near infrared reflectance spectroscopy,NIRS)监测幼猪CPB模型中rSO_2的变化。在CPB开始前10 min、CPB开始后10 min、升主动脉阻断后30 min和升主动脉开放后10 min 4个时间点检测血清S100钙结合蛋白B(S100 B)浓度。分别进行苏木精-伊红(HE)染色、尼氏染色观察海马CA区组织学变化。结果在主动脉阻断期间,H组脑灌注流量[(30.8±9.9)mL/(kg·min)]较L组[(19.0±7.4)mL/(kg·min)]有增高趋势但无统计学差异(P=0.072),且该时间点H组rSO_2值(52.65%±3.1%)显著高于L组(47.3%±3.3%)(P0.05)。海马组织学变化及血清S100 B蛋白水平无组间差异。结论在小型猪体外循环灌注模型中,脑动脉内流量及局部脑氧饱和度监测提示脑血流压力/血流自我调节减弱,高流量组脑灌注效果优于低流量灌注。     

血流动力学的医学应用与发展

血流动力学是指血液在血管系统中流动的力学,主要研究血流量、血流阻力、血压、切应力、扰动流等,以及它们之间的相互关系,对人类生命健康具有重要的影响。血流动力学在血管的弯曲、狭窄、堵塞、分叉以及肿瘤的治疗等方面具有重要的临床研究意义。目前,血流动力学在动脉血管搭桥、冠状动脉狭窄、腹主动脉瘤、动脉粥样硬化、脑动脉肿瘤以及旋动流等方面引起广泛研究。伴随着血流动力学的深入研究,心脑血管的手术规划、介入治疗等得到快速发展,基于血流动力学的临床检测和治疗仪器也越来越多。血流动力学因素,如血管压力、血管阻力、血流量、壁面切应力、血液黏度、流动分离、湍流、涡流等对常见血管疾病以及术后并发症的影响机理正在逐步深入探索之中,并已经取得了一定成果。     

Impaired cerebral and systemic hemodynamics under cognitive load in young hypotensives: a transcranial Doppler study

Reduced sympathetic outflow and deficits in cerebral hemodynamics have been considered as possible factors mediating the impaired cognitive performance in essential hypotension. However, the relationship between systemic blood pressure (BP), cerebral blood flow and cognitive functioning is still poorly understood. The present study was aimed at clarifying the physiological processes underlying cerebral and systemic hemodynamics in young hypotensives during cognitive engagement. Doppler sonography blood flow velocities in both middle cerebral arteries were measured from 17 hypotensives and 15 normotensives during a working memory task. Impedance cardiographic and BP measures were also recorded continuously. Lower increases in systolic and diastolic BP were observed in hypotensives. However, no evidence of lower sympathetic control was found for this group, as assessed by pre-ejection period. Flow velocity in middle cerebral arteries showed a lower increase in hypotensives throughout the task. Moreover, significant positive correlations between BP changes and blood flow velocities in middle cerebral arteries during the task were obtained for this group only, suggesting a less effective cerebral autoregulation. No difference was found between groups in task performance. Results suggest that during cognitive challenge hypotensives show impaired hemodynamic adjustments, both central and peripheral. However, such alterations do not directly affect cognitive performance, at least under moderate cognitive load.     

Cerebrovascular response during and following severe insulin-induced hypoglycemia: CO2-sensitivity,autoregulation, and influence of prostaglandin synthesis inhibition

The objective of the present experiments was to study mechanisms governing cerebrovascular responses during severe hypoglycemia, and in the posthypoglycemic recovery period. To that end, lightly anesthetized (70% N₂O) and artificially ventilated rats were injected with insulin so as to abolish spontaneous EEG activity for 15 or 30 min (“coma”). In separate animals, recovery was induced by glucose administration. Previous experiments have shown that in normo- or moderately hypertensive animals hypoglycemic coma is accompanied by a relatively marked increase in cerebral blood flow (CBF), and that a delayed hypoperfusion develops in the recovery period. The present results demonstrate that oxygen supply is in excess of the demands during coma, and falls below control during recovery. During hypoglycemic coma, the CO₂ response of the circulation was retained but autoregulation was lost. In the recovery period, both CO₂ response and autoregulation were lost. Pretreatment with indomethacin was introduced in order to evaluate the possible influence of fatty acid cyclo-oxygenase products on the pattern of CBF changes. Measurements of local cerebral blood flow (1-CBF) showed that, in the majority of structures analysed, indomethacin failed to modulate the changes in CBF. It is concluded that alterations in cerebrovascular tone and loss of autoregulation induce flow changes that may influence substrate and oxygen availability during hypoglycemia. The pronounced decrease in CBF and the loss of autoregulation and CO₂-response in the posthypoglycemic period may influence functional, metabolic and morphological recovery. The 1-CBF findings indicate that neither the increase in CBF during hypoglycemia nor the reduction in flow in the posthypoglycemic period are mediated by mechanisms related to prostaglandin metabolism.     

Prenatal stress and hemodynamics in pregnancy: a systematic review

Maternal prenatal stress is associated with preterm birth, intrauterine growth restriction, and developmental delay. However, the impact of prenatal stress on hemodynamics during pregnancy remains unclear. This systematic review was conducted in order to assess the quality of the evidence available to date regarding the relationship between prenatal stress and maternal–fetal hemodynamics. The PubMed/Medline, EMBASE, PsycINFO, Maternity and Infant Care, Trip, Cochrane Library, and CINAHL databases were searched using the search terms pregnancy; stress; fetus; blood; Doppler; ultrasound. Studies were eligible for inclusion if prenatal stress was assessed with standardized measures, hemodynamics was measured with Doppler ultrasound, and methods were adequately described. A specifically designed data extraction form was used. The methodological quality of included studies was assessed using well-accepted quality appraisal guidelines. Of 2532 studies reviewed, 12 met the criteria for inclusion. Six reported that prenatal stress significantly affects maternal or fetal hemodynamics; six found no significant association between maternal stress and circulation. Significant relationships between prenatal stress and uterine artery resistance (RI) and pulsatility (PI) indices, umbilical artery RI, PI, and systolic/diastolic ratio, fetal middle cerebral artery PI, cerebroplacental ratio, and umbilical vein volume blood flow were found. To date, there is limited evidence that prenatal stress is associated with changes in circulation. More carefully designed studies with larger sample sizes, repeated assessments across gestation, tighter control for confounding factors, and measures of pregnancy-specific stress will clarify this relationship.     

Structural MRI of carotid artery atherosclerotic lesion burden and characterization of hemispheric cerebral blood flow before and after carotid endarterectomy

Collateral circulation plays a major role in maintaining cerebral blood flow (CBF) in patients with internal carotid artery (ICA) stenosis. CBF can remain normal despite severe ICA stenosis, making the benefit of carotid endarterectomy (CEA) or stenting difficult to assess. Before and after surgery, we assessed CBF supplied through the ipsilateral (stenotic) or contralateral ICA individually with a novel hemisphere-selective arterial spin-labeling (ASL) perfusion MR technique. We further explored the relationship between CBF and ICA obstruction ratio (OR) acquired with a multislice black-blood imaging sequence. For patients with unilateral ICA stenosis (n = 19), conventional bilateral labeling did not reveal interhemispheric differences. With unilateral labeling, CBF in the middle cerebral artery (MCA) territory on the surgical side from the ipsilateral supply (53.7 +/- 3.3 ml/100 g/min) was lower than CBF in the contralateral MCA territory from the contralateral supply (58.5 +/- 2.7 ml/100 g/min), although not statistically significant (p = 0.09). The ipsilateral MCA territory received significant (p = 0.02) contralateral supply (7.0 +/- 2.7 ml/100 g/min), while ipsilateral supply to the contralateral side was not reciprocated. After surgery (n = 11), ipsilateral supply to the MCA territory increased from 57.3 +/- 5.7 to 67.3 +/- 5.4 ml/100 g/min (p = 0.03), and contralateral supply to the ipsilateral MCA territory decreased. The best predictor of increased CBF on the side of surgery was normalized presurgical ipsilateral supply (r(2) = 0.62, p = 0.004). OR was less predictive of change, although the change in normalized contralateral supply was negatively correlated with OR(excess) (=OR(ipsilateral) - OR(contralateral)) (r(2) = 0.58, p = 0.006). The results demonstrate the effect of carotid artery stenosis on blood supply to the cerebral hemispheres, as well as the relative role of collateral pathways before surgery and redistribution of blood flow through these pathways after surgery. Unilateral ASL may better predict hemodynamic surgical outcome (measured by improved perfusion) than ICA OR.     

Model-based physiomarkers of cerebral hemodynamics in patients with mild cognitive impairment

In our previous studies, we have introduced model-based “functional biomarkers” or “physiomarkers” of cerebral hemodynamics that hold promise for improved diagnosis of early-stage Alzheimer's disease (AD). The advocated methodology utilizes subject-specific data-based dynamic nonlinear models of cerebral hemodynamics to compute indices (serving as possible diagnostic physiomarkers) that quantify the state of cerebral blood flow autoregulation to pressure-changes (CFAP) and cerebral CO2 vasomotor reactivity (CVMR) in each subject. The model is estimated from beat-to-beat measurements of mean arterial blood pressure, mean cerebral blood flow velocity and end-tidal CO2, which can be made reliably and non-invasively under resting conditions. In a previous study, it was found that a CVMR index quantifying the impairment in CO2 vasomotor reactivity correlates with clinical indications of early AD, offering the prospect of a potentially useful diagnostic tool. In this paper, we explore the use of the same model-based indices for patients with amnestic Mild Cognitive Impairment (MCI), a preclinical stage of AD, relative to a control subjects and clinical cognitive assessments. It was found that the model-based CVMR values were lower for MCI patients relative to the control subjects.     

Control and autoregulation of the blood circulation in the vertebrobasilar system.

The author establishes an analogy between the control mechanism and autoregulation of the cerebral blood flow and the protection of the vascular wall of the internal carotid artery constituted by the conjunction of the 'internal carotid-cavernous sinus' system with the 'vertebrobasilar-transverse-occipital dural sinus or basilar' 'sinus' system (an extension of the cavernous sinus) in the autoregulation and control of the encephalic circulation carried out through this latter vessel, together with the protection of its vascular walls. The author believes it to be very difficult to demonstrate in practice the functioning of these mechanisms, but he argues that the unusual anatomical features of the systems are indicative of their particular physiological roles.     

Autoregulation of the cerebral circulation during sleep in newborn lambs

Autoregulation is a vital protective mechanism that maintains stable cerebral blood flow as cerebral perfusion pressure changes. We contrasted cerebral autoregulation across sleep–wake states, as little is known about its effectiveness during sleep. Newborn lambs ( n = 9) were instrumented to measure cerebral blood flow (flow probe on the superior sagittal sinus) and cerebral perfusion pressure, then studied during active sleep (AS), quiet sleep (QS) and quiet wakefulness (QW). We generated cerebral autoregulation curves by inflating an occluder cuff around the brachiocephalic artery thereby lowering cerebral perfusion pressure. Baseline cerebral blood flow was higher ( P < 0.05) and cerebral vascular resistance lower ( P < 0.05) in AS than in QW (76 ± 8% and 133 ± 15%, respectively, of the AS value, mean ± s.d. ) and in QS (66 ± 11% and 158 ± 30%). The autoregulation curve in AS differed from that in QS and QW in three key respects: firstly, the plateau was elevated relative to QS and QW ( P < 0.05); secondly, the lower limit of the curve (breakpoint) was higher ( P < 0.05) in AS (50 mmHg) than QS (45 mmHg); and thirdly, the slope of the descending limb below the breakpoint was greater ( P < 0.05) in AS than QS (56% of AS) or QW (56% of AS). Although autoregulation functions in AS, the higher breakpoint and greater slope of the descending limb may place the brain at risk for vascular compromise should hypotension occur.