轻型头部损伤后脑血流的自动调节

脑血流自动调节是指在血压变化时脑循环有能力维持相对恒定的血流量。本文研究的目的是确定当头部受轻度损伤时脑血流自动调节功能是否受到损害。对29例轻型头部损伤GCS(Glasgow Coma Scale)评分为13～15的伤员,用经颅多普勒持续48h监测血流速度,并记录血压,以测定其脑血流自动调节功能。29例年龄相当的志愿者也以同样方式测定了脑血流自动调节功能,作为对照值。在短暂的动脉血压变化情况下测定脑血流速度及计算出自动调节指数,以评估自动调节功能。     

TCD结合体位改变对脑血流自动调节评估在神经系统疾病中的应用价值

脑血流自动调节(Cerebral autoregulation,CA)是指脑血流在动脉血压(Arterial blood pressure,ABP)和脑灌注压(Cerebral perfusion pressure,CPP)发生改变时保持相对稳定的能力.临床通过改变血压后测量脑血流的变化以反映CA的方式有很多,如:大腿袖带、下肢负压、冷加压试验,握拳动作、Valsalva动作等.经颅多普勒超声(Transcranial Doppler,TCD)是在生理和病理情况下测定脑血流速度和脑自动调节能力的有效工具[1],它结合体位改变对脑血流进行测量是一种更方便更易接受的方法,不论对卒中预后进行评估还是某些自主神经疾病的辅助诊断方面,均发挥了重要作用.     

一氧化氮在脑血流自动调节中的作用

<正>脑血流自动调节是指全身动脉血压发生变化和因而产生的脑灌注压在一个较大范围内发生变化时,脑通过调节脑小血管的口径使脑血管阻力发生相应变化,从而使脑血流量维持恒定的一个复杂的多因素过程。在调控脑血流自动调节的复杂的机制中,一氧化氮作为重要的血管舒张因子,其作用不容忽视[1-2]。本文重点介绍一氧化氮在脑血流自动调节中的作用、与常见脑血管病的关系及研究前景。     

脑血流自动调节及神经血管耦联机制在颈动脉支架围术期的应用研究进展

脑血流自动调节（cerebral autoregulation,CA）系指在一定血压或脑灌注压波动范围内,通过脑小血管的舒缩功能维持脑血流量（cerebral blood flow,CBF）相对稳定的能力。缺血性脑血管相关疾病可导致脑血流自动调节功能受损,其相关机制尚不明确。针对二者关系的研究是当前热点,CA及神经血管耦联（neurovascular coupling,NVC）在颈动脉支架围术期的监测同样发挥着重要价值。本文主要就CA和NVC在颈动脉支架围术期监测的相关进展做一综述,旨在探讨CA及NVC在颈动脉支架围术期进行脑血流自动调节功能监测的临床应用价值。     

脑血流自动调节监测在脑血管疾病中的临床应用

脑血流自动调节（cerebral autoregulation,CA）是指脑血流在动脉血压（arterial blood pressure,ABP）和脑灌注压（cerebral perfusion pressure,CPP）发生改变时保持相对稳定的能力。临床主要通过改变血压后测量脑血流的变化以反映CA的方式很多,常用的有：下肢负压、冷加压试验、Valsalva动作等。通过改变脑灌注压来评估CA能力主要由经颅多普勒超声（transcranial Doppler,TCD）来实现,它是在生理和病理情况下测定脑血流速度和CA的有效工具,它结合体位改变对脑血流进行测量是一种更方便、更易接受的方法,对缺血性脑血管病的预后评估起到重要作用。本文就CA监测在脑血管疾病中的临床应用做一综述。     

血压波动对脑梗死后脑灌注的影响

本文主要从脑血管的自动调节与自动调节受损、脑小血管病变可导致脑血管反应性受损、脑梗死患者脑血流速度、脑血流量与血压的相关性,脑梗死侧大脑半球脑灌注降低、低血压对脑主要动脉狭窄者可导致狭窄远端脑组织局部低灌注等几个方面来讨论脑梗死后血压的变化对脑血流速度、脑血流量的影响。给临床医生提出一个思考问题,在脑梗死的急性期把血压控制在多少才是最合适的水平,对患者的功能恢复最有益。     

一氧化氮与脑缺血及实验性脑保护治疗

自从Furchgott等在1980年从离体血管中发现一氧化氮（NO）后，众多学者逐渐阐明了NO在心脑血管等多个系统参与多种生理功能调节及多种疾病的病理过程。现就其在脑缺血中的作用综述如下。一、NO对脑血管及血流的调节NO是一种活性极高的气体分子，亲脂性强，易透过生物膜扩散到血管内皮下平滑肌及血管腔内，产生多种生物学效应，因而在调节脑血管舒缩活动、改善脑血流方面起着十分重要的作用。NO调整血管功能，参与大鼠血压节律性波动调节[1]。其不仅舒张脑内大、小动脉，且对静脉也有舒张作用。机制是通过L精氨酸-NO-环磷酸鸟苷通路，…     

脑血流自动调节研究发展史

脑血流自动调节系指在全身血压波动的情况下脑血流量保持相对恒定的能力。脑血流自动调节相关研究迄今已有近百年历史,从动物模型到无创性在体实时脑血流动力学监测,检测技术的进步特别是经颅多普勒超声的广泛应用和数学建模方法的引入,为脑血流自动调节研究带来了革新。本文旨在总结脑血流自动调节机制及检测技术的发展史,以为临床开展相关研究提供参考。     

脑血流自动调节概述及其在脑血管疾病中的应用

<正>脑是人体代谢率最高的器官,由于脑的新陈代谢旺盛、生理功能复杂,所以脑的血液供应必须十分丰富,稳定、充足的脑血流量对脑功能的正常发挥和脑的高代谢水平的维持是极其重要的。脑血流自主调节功能是维持脑血流量的重要因素之一。有研究表明,许多脑部疾病(如脑卒中、痴呆、偏头痛、脑外伤等)的脑血流自动调节功能均有不同程度的改变[1,2]。因此,了解脑血流自动调节功能对疾病诊治有着极其重要的作用。     

临界关闭压对于正常大鼠脑血流自动调节的作用

目的 探讨正常大鼠脑血流自动调节范围内和超出自动调节范围后,临界关闭压（critical closing pressure,CCP）对脑血流的调控作用。 方法 健康雄性SD大鼠随机分为升压组和降压组各70只,除去手术失败的动物,完整采集数据升压 组69只,降压组54只。分别以10～15 mmHg为一级逐步升高、降低血压,同步记录大鼠大脑中动脉血 流速度（cerebral blood flow velocity,CBFV）和有创血压,绘制自动调节曲线,并按照CCP理论计算CCP 和血管面积阻力指数（resistance area product,RAP）,分析血流动力参数之间,以及血流动力学参数 与血压变化间的关系。 结果 动脉血压升高或降低过程中,正常大鼠的脑血流自动调节上、下限分别为（148.12±7.49）mmHg、 （62.96±3.34）mmHg。脑血流自动调节范围内,CBFV随动脉血压改变轻微,超出自动调节范围后,CBFV 随动脉血压升高明显增加（r =0.896,P =0.000）,或随动脉血压降低明显减小（r =0.945,P＜0.001）。 CCP变化恰好与CBFV相反,自动调节范围内随动脉血压改变明显,与平均动脉压呈明显正相关（升压 r =0.967、降压r =0.969,P均＜0.001）,超出自动调节范围后改变量明显减小。RAP也有CCP的类似趋势, 但数值变化量不是很明显,只有降压过程自动调节范围内的改变量明显大于超出自动调节范围后。 结论 大鼠脑血流调控过程中,自动调节有效范围内,脑血流的稳定与CCP和RAP密切相关,尤其是 CCP。微动脉血管紧张度和微动脉直径变化共同参与了脑血流的调控。     

静息状态的动态脑血流自动调节：检查方法及临床应用

CA是维持脑血流恒定的生理机制。测量CA的方法很多。本文要介绍的是在静息状态下， 利用传递函数计算外围动脉血压和脑血流间的低频相位差，即可测量CA。CA和脑血管疾病的预后有 关，因此它有潜力成为有用的临床诊疗工具。     

Multimodality monitoring during passive tilt and Valsalva maneuver under hypercapnia.

In occlusive cerebrovascular disease cerebral blood flow (CBF) autoregulation can be impaired and constant CBF during fluctuations in blood pressure (BP) cannot be guaranteed. Therefore, an assessment of cerebral autoregulation should consider not only responsiveness to CO2 or Diamox. Passive tilting (PT) and Valsalva maneuver (VM) are established tests for cardiovascular autoregulatory function by provoking BP changes. To develop a comprehensive test for vasomotor reactivity with a potential increase of sensitivity and specificity, the authors combined these maneuvers. Blood pressure, corrected to represent arterial pressure at the level of the circle of Willis, middle cerebral artery Doppler frequencies (DF), heart rate (HR) and endtidal partial pressure of CO2 (PtCO2) were measured continuously and noninvasively in 81 healthy subjects (19-74 years). Passive tilt and Valsalva maneuver were performed under normocapnia (mean, 39 + 4 mmHg CO2) and under hypercapnia (mean, 51 + 5 mm Hg CO2). Resting BP, HR, and DF increased significantly under hypercapnia. Under normocapnia and hypercapnia, PT induced only minor, nonsignificant changes in mean BP at the level of the circle of Willis compared to baseline (normocapnia: + 2 + 15 mm Hg; hypercapnia: -3 +/- 13 mm Hg). This corresponded with a nonsignificant decrease of the mean of DF (normocapnia: -4 +/- 11%; hypercapnia -6 +/- 12%). Orthostasis reduced pulsatility of BP by a predominantly diastolic increase of BP without significant changes in pulsatility of DF. Valsalva maneuver, with its characteristic rapid changes of BP due to elevated intrathoracic pressure, showed no significant BP differences in changes to baseline between normocapnic and hypercapnic conditions. Under both conditions the decrease in BP in phase II was accompanied by significantly increased pulsatility index ratio (PIDF/PIBP). Valsalva maneuver and PT as established tests in autonomic control of circulation provoked not only changes in time-mean of BP but also in pulsatility of BP. The significant increase in pulsatility ratio and decrease of the DF/BP ratio during normocapnia and hypercapnia indicated preserved CBF autoregulation within a wide range of CO2 partial pressures. Hypercapnia did not significantly influence the autoregulatory indices during VM and PT. Physiologically submaximally dilated cerebral arterioles can guarantee unchanged dynamics of cerebral autoregulation. Combined BP and MCA-DF assessment under hypercapnia enables investigating the effect of rapid changes of blood pressure on CO2-induced predilated cerebral arterioles. Assuming no interference of hypercapnia-induced vasodilation, VM, with its rapid, distinct changes in BP, seems especially to be adequate provocation for CBF autoregulation. This combined vasomotor reactivity might provide a more sensitive diagnostic tool to detect impaired cerebral autoregulation very early.     

特发性高颅压患者脑血流自动调节研究

目的 分析特发性颅内压增高（idiopathic intracranial hypertension，IIH）患者脑血流自动调节机能。
方法 连续入组2018年12月-2019年3月在首都医科大学附属北京天坛医院就诊的IIH患者，并选取年
龄匹配的健康志愿者作为对照组。应用传递函数的算法分析TCD显示的大脑中动脉血流速度及动脉
血压的自然波动以评估脑血流自动调节机能。
结果 入组IIH组10例，对照组13例。所有入组者均完成了双侧大脑半球的脑血流自动调节检测，共
检测了20个高颅压半球及26个正常对照半球。与对照组相比，IIH组大脑中动脉脑血流增益显著降
低[（0.64±0.35）%/% vs（0.37%±0.20）%/%，P =0.004]；相位也显著降低（58.80±20.86°vs
39.16±23.79°，P =0.005），差异有统计学意义。IIH组每秒钟脑血流速度的恢复率较对照更低，但差
异尚未达到统计学意义（[ 26.34±43.29）%/s vs（38.81±20.16）%/s，P=0.240]。
结论 IIH患者脑血流自动调节机能显著受损。     

脑梗死急性期患者脑血流自动调节功能观察

目的 利用临界关闭压（critical closing pressure,CCP）探讨脑梗死急性期自动调节功能及与病情的相关性。      

Reduced cerebral blood flow velocity and impaired cerebral autoregulation in patients with Fabry disease

Abstract. In Fabry disease, there is glycosphingolipid storage in vascular endothelial and smooth muscle cells and neurons of the autonomic nervous system. Vascular or autonomic dysfunction is likely to compromise cerebral blood flow velocities and cerebral autoregulation. This study was performed to evaluate cerebral blood flow velocities and cerebral autoregulation in Fabry patients. In 22 Fabry patients and 24 controls, we monitored resting respiratory frequency, electrocardiographic RR-intervals, blood pressure, and cerebral blood flow velocities (CBFV) in the middle cerebral artery using transcranial Doppler sonography. We assessed the Resistance Index, Pulsatility Index, Cerebrovascular Resistance, and spectral powers of oscillations in RR-intervals, mean blood pressure and mean CBFV in the high (0.15–0.5 Hz) and sympathetically mediated low frequency (0.04–0.15 Hz) ranges using autoregressive analysis. Cerebral autoregulation was determined from the transfer function gain between the low frequency oscillations in mean blood pressure and mean CBFV. Mean CBFV (P < 0.05) and the powers of mean blood pressure (P < 0.01) and mean CBFV oscillations (P < 0.05) in the low frequency range were lower,while RR-intervals, Resistance Index (P < 0.01), Pulsatility Index, Cerebrovascular Resistance (P < 0.05), and the transfer function gain between low frequency oscillations in mean blood pressure and mean CBFV (P < 0.01) were higher in patients than in controls. Mean blood pressure, respiratory frequency and spectral powers of RR-intervals did not differ between the two groups (P > 0.05). The decrease of CBFV might result from downstream stenoses of resistance vessels and dilatation of the insonated segment of the middle cerebral artery due to reduced sympathetic tone and vessel wall pathology with decreased elasticity. The augmented gain between blood pressure and CBFV oscillations indicates inability to dampen blood pressure fluctuations by cerebral autoregulation. Both, reduced CBFV and impaired cerebral autoregulation, are likely to be involved in the increased risk of stroke in patients with Fabry disease.     

Challenging cerebral autoregulation in patients with preganglionic autonomic failure

Intact cerebral autoregulation is essential to prevent cerebral hypoperfusion during pronounced changes in arterial blood pressure (ABP) in patients with autonomic failure (AF). It is still a matter of debate whether and to what extent cerebral autoregulation is disturbed in these patients. This study evaluates the interaction between cerebral blood flow velocity (CBFV) and ABP during Valsalva maneuver (VM) and tilt-table testing in nine patients with multiple system atrophy including AF and in 14 age-matched controls. CBFV and ABP were recorded noninvasively using transcranial Doppler sonography and the Finapres device. Responses to VM were graded by the autoregulation slope index (ASI). Cerebrovascular resistance changes were estimated by the conventional ratio ABP/CBFV and by the dynamic pressure-velocity relationship. To challenge cerebral autoregulation further, tests were repeated under hypercapnic predilation of cerebral arterioles. During VM, CBFV reincreased in patients despite a pronounced ABP drop and showed an overshoot after the strain, thus, being similar to controls. The ASI was higher in patients than in controls ( p < 0.05). During 70 degrees head-up tilt, ABP dropped markedly, but the decrease in CBFV was small and did not differ significantly from controls. In patients, both tests were associated with a substantial decrease of the dynamic but not of the conventional pressure-velocity relationship. Under hypercapnia, the CBFV response in patients remained unchanged. We conclude that 1). cerebral arterioles have the capacity for adequate vasodilation during ABP drops in patients with AF and that this ability is still present under hypercapnic predilation. 2). The mechanism of cerebral autoregulation in itself does not seem to be affected by the AF but is rather well exercised. 3) The VM presents, in addition to tilt-table testing, a simple test for clinical evaluation of cerebral autoregulation in patients with AF.     

Dynamic cerebral autoregulation testing as a diagnostic tool in patients with carotid artery stenosis

Evaluation of dynamic cerebral autoregulation might yield a physiologically more adequate measure of cerebral hemodynamic impairment in carotid artery stenosis than CO2-reactivity. This study re-evaluates and compares the Valsalva maneuver (VM) and phase shift during deep breathing. Nineteen patients with severe carotid artery stenosis and 17 age-matched controls were examined using transcranial Doppler sonography and non-invasive blood pressure recordings (Finapres). Phase shift was determined by cross-spectral analysis, responses to VM were graded by the formerly-introduced autoregulation slope index (ASI) and the new Valsalva time index (VTI). Phase shift and autoregulatory indices were significantly reduced on the affected side (p < 0.001). Correlations with CO2-reactivity were significant when pooling values of controls and patients (r from 0.54 to 0.78; p < 0.001). Correlations except for the VTI (r = -0.65; p = 0.002) were not significant considering only the affected side in patients. Correlations of pooled values between phase shift and VM-derived indices were significant (VTI r = -0.62; p < 0.001; ASI r = 0.49; p < 0.001), within patients only when comparing side-to-side differences (VTI r = -0.58; p = 0.009; ASI r = 0.52; p = 0.023). In conclusion, detection of impaired cerebral autoregulation is possible both by deep breathing and VM. The new VTI seems to be more suitable than the conventional ASI. Inter-method agreement concerning the extent of impairment is only acceptable for intra-individual side-to-side differences. Since absolute values of one autoregulation testing method or CO2-reactivity alone might fail, various tests should be combined for comprehensive assessment of cerebral hemodynamic impairment.     

Mechanisms of cerebral autoregulation, assessment and interpretation by means of transcranial doppler sonography

Cerebrovascular autoregulation assures constancy of cerebral perfusion despite blood pressure changes, as long as mean blood pressure remains in a range between 50-170 mmHg. Static and dynamic myogenic mechanisms dampen sudden blood pressure changes. Neurogenic influences of sympathetic, noradrenergic fibers modulate primarily proximal, large diameter segments of cerebral arteries, but also small 15-20 microns diameter vessels. Parasympathetic, vasodilating impulses are of less influence. Monoaminergic brainstem centers such as the dorsal raphe nucleus, locus coeruleus or nucleus reticularis pontis oralis also influence vessel tone. Metabolic, local parenchymal and endothelial substances have major impact on cerebral vessel tone. Particularly important are nitric oxide, calcitonin gene related peptide, substance P, endothelin, potassium channels and autocoids such as histamine, bradykinin, arachidonic acid, prostanoids, leucotrienes, free radicals or serotonin. The clinical examination of autoregulation is mostly based on brief blood pressure changes induced by drugs such as angiotensin, phenylephrine or sodium nitroprusside, or by challenge maneuvers. Frequently, blood pressure is challenged by a tilt-table maneuver, the "leg-cuff"-method according to Aaslid, or a Valsalva maneuver. The analysis of coherence and phase relation between spontaneous or metronomic breathing modulation of blood pressure and brain perfusion also assesses autoregulatory function. Cerebral blood flow is determined by means of transcranial Doppler sonography, mostly of the proximal segment of the mid-cerebral artery. There is some controversy whether a decrease of cerebral blood flow velocity measured at this segment indicates vasodilatation at the insonated segment or reflects blood flow reduction due to decreased perfusion of down-stream vessel segments. Various clinical and animal studies are presented demonstrating diameter constancy of the insonated mid-cerebral artery segment and thus indicating that slowing of mid cerebral artery blood flow velocity as assessed by transcranial Doppler sonography is due to a decrease of down-stream perfusion. Direct, intraoperative measurements of vessel diameter confirm this conclusion.