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。     

临界关闭压在脑血流动力学评价中的应用

目的探讨检测脑血流动力学的快捷、实用的新方法,为临床检测奠定基础。方法利用经颅多普勒(TCD)检测大鼠大脑中动脉(MCA)的血流速度,同步记录有创血压,按照临界关闭压(CCP)的理论计算出脑血流自动调节的下限和微动脉阻力,与改变血压测定的结果进行比较。结果CCP法检测到的脑血流自动调节下限为70.88±24.05mmHg,与常用血压改变测定的结果数值接近,可以相互替代。肾血管性高血压大鼠(RHR)的脑血流自动调节下限和微动脉阻力的升高,与动脉血压的升高,特别是脉压差的增大密切相关。结论按照CCP理论测定脑血流自动调节下限和微动脉的阻力,可以准确、快捷地反映脑血流动力学的生理状态和病理改变。     

临界关闭压对高血压大鼠脑血流的调控作用

目的 探讨临界关闭压（critical closing pressure,CCP）对肾血管性高血压大鼠（renovascular hypertensive rats,RHR）脑血流动力学改变的调控作用。方法 RHR模型（RHR组）26只,假手术正常血压对照组24只,同步记录大脑中动脉血流速度（cerebral blood flow velocity,CBFV）和有创血压,按照CCP理论计算CCP和小动脉阻力,并分析血流动力学参数之间,以及血流动力学参数与血管形态参数改变间的关系。结果 与对照组比较,RHR组动脉血压明显升高的同时,脑循环有效灌注压（effective cerebral perfusion pressure,CPPe）和血管面积阻力指数（resistance area product,RAP）明显升高（CPPe：100.80±26.40 mmHg vs 67.30±13.10 mmHg,P<0.01;RAP：2.94±0.85 vs 2.30±0.59,P=0.003）,但CBFV相对稳定,脑循环阻力（cerebral vascular resistance,CVR）升高不明显。RHR组血管面积阻力指数（resistance area product,RAP）只与小动脉管腔内径呈负相关（rs=-0.610,P=0.001）,CCP与小动脉中膜厚度呈正相关（rs=0.554,P=0.006）;而CVR不仅与小动脉管腔内径呈负相关（rs=-0.463,P=0.023）,也与小动脉中膜厚度呈正相关（rs=0.678,P＜0.01）。结论 RHR的脑血流调控可通过CCP和RAP的改变来完成,用CCP和RAP代替CVR,能更加真实、客观地反映脑血流动力学的调控机制。     

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.     

脑血管病患者的脑血流自身调节潜力分析

目的 应用TCD和倾斜试验评价脑血管病患者的脑血流自身调节.方法 脑血管狭窄患者32例(A组),无血管狭窄的脑梗死患者28例(B组),健康对照26名.通过呼吸试验计算呼吸抑制指数(BHI)及血管运动反应性(VMR)评价脑小血管CO2反应性;头高位70°倾斜试验改变体位,记录卧立位脑血流速度(CBFV)及血压、心率,评价脑小血管的血压-自动调节.结果 与对照组比较,A组、B组VMR(分别为0.18±0.02和0.26±0.04,对照组为0.43±0.06)、BHI(分别为0.76±0.15和1.05±0.15,对照组为1.52±0.19)显著降低(P＜0.05).A组患侧与对侧VMR(分别为0.10±0.01、0.22±0.02)及BHI(分别为0.51±0.14、0.94±0.16),差异有统计学意义(P＜0.05).A组患侧BHI值小于0.69(P＜0.05).Logistic回归分析显示BHI下降与脑梗死相关(B=2.234,P=0.016).直立位时血压、心率增加,CBFV下降.3例直立性低血压患者直立位血压和CBFV均显著下降,二者之间相关(r=0.430,P=0.004).结论 脑梗死及脑血管狭窄患者脑小血管CO2反应性受损.自身调节能力受损,卒中风险可能增加.直立位时,机体通过提高周围血压和心率,参与颅内自动调节.     

缺血性脑卒中的脑血流调节研究进展

<正>脑血流自动调节(cerebral autoregulation,CA)是大脑的一种内在保护机制,它能在动脉血压或脑灌注压在一定范围内波动时保证相对稳定的脑血流(cerebral blood flow,CBF)~([1])。CA是一种快速调节机制,通过调节脑血管阻力,补偿脑灌注压力的波动,维持相对稳定的脑血流~([2,3])。CA分     

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。     

脑血管自动调节能力的参数评估

脑血管自动调节功能是脑血管自身具备的一种在动脉血压(arterial blood pressure,ABP)或脑灌注压(cerebral perfusion pressure,CPP)发生改变时保持脑血流动力学稳定性的能力,是一种用于预防继发性缺血损伤的内在保护机制[1-2].     

不同亚型急性缺血性卒中动态脑血流自动调节的研究

背景根据急性卒中治疗低分子肝素试验病因分型法(Trial of Org 10172 in Acute Stroke Treatment,TOAST),大动脉粥样硬化性卒中和小动脉闭塞性卒中是缺血性卒中的主要类型。这两种卒中亚型的临床特征和预后不同,可能与其影响动态脑血流自动调节功能(dynamic cerebral autoregulation,d CA)的不同机制有关。因此,本研究针对两种卒中亚型的d CA展开。方法收集了41例单侧大脑中动脉供血区的急性缺血性卒中患者(15例大动脉粥样硬化性卒中和26例小动脉闭塞性卒中)和20例健康志愿者。分别通过经颅多普勒超声(transcranial Duplex,TCD)来监测双侧大脑中动脉血流速度(cerebral blood flow velocity,CBFV)和指尖血压监测法监测中指的连续血压。通过传递函数来分析脑血流自动调节(cerebral autoregulation,CA)的相关参数:相位差(phase difference,PD)、增益(gain)和阶跃响应(slope of step response)。结果在大动脉粥样硬化性卒中组,病变半球的PD明显低于非病变半球(42.9°±18.5°vs72.4°±29.9°,P0.01),非病变半球与健康对照组PD比较,差异无显著性(P0.1);在小动脉闭塞性卒中组,病变半球与非病变半球的PD比较差异无显著性(33.8°±17.9°vs 32.6°±21.1°,P0.1),且双侧均显著低于健康对照组(P0.001)。阶跃响应结果与PD相似。结论不同亚型的急性缺血性卒中的d CA不同,可能与脑血管的不同病理改变有关。     

下肢袖带释放实验在脑血流自动调节评估中的应用现状

下肢袖带释放实验（thigh c uffs r elease t est，TCRT）是由Rune A aslid于1989年首先提出， 在双侧大腿绑上袖带，先充气，后快速放气，使血液重新汇集于双侧大腿，造成动脉血压（arterial blood pressure，ABP）与脑血流速度（cerebral blood flow velocity，CBFV）急骤下降，同时记录ABP和 CBFV的变化，进而评估dCA，是评估dCA常用诱发方法之一。目前临床上TCRT多应用于急性缺血性卒中、 头外伤、重度子痫等的dCA评估。该方法具有价廉、简便、无创、可重复等优势。本文就TCRT在dCA评估 中的应用现状做一简要综述。     

Autoregulation of cortical blood flow and oxygen tension in the rabbit

The relationship between cerebral blood flow autoregulation and oxygen tension of cerebral tissue is not fully known. We have examined the autoregulation of local cortical blood flow (CoBF) and cortical oxygen tension (bP_O2) in the rabbit.

CoBF was measured continuously by using the heated thermocouple technique and bP_O2 was monitored by the polarographic method. Intravenous injection of phenylephrine hydrochloride or trimethaphan camsylate was used to test for autoregulation by increasing or decreasing perfusion pressure. The mean values of CoBF and bP_O2 were 36±5 ml/100g/min and 32±12 mmHg respectively at 90 mmHg mean arterial blood pressure (MABP). The changes in both CoBF and bP_O2 with changing perfusion pressure were often relatively small at near baseline blood pressure and became more pronounced with large increases or decreases in MAPB. On returning from high MABP to baseline blood pressure, a hysteresis effect on CoBF was observed in 20 out of 22 cases.

The autoregulation of CoBF was maintained in the range between 80 and 100 mmHg MABP. On the other hand, bP_O2 was maintained constant in the range between 80 and 110 mmHg. This range is significantly wider than that of CoBF. We conclude that autoregulation of CoBF limits changes in local CoBF to maintain constant oxygen tension in brain tissue.     

Autoregulation and CO2 response of cortical blood flow and their relation to cortical oxygen tension

Autoregulation and CO2 response of cortical blood flow and their relationship to cortical oxygen tension is not fully known. We have examined autoregulation and CO2 response of local cortical blood flow (CoBF) and cortical oxygen tension (bPO2), using 41 New Zealand white rabbits. CoBF was measured continuously by using the heated thermocouple technique and bPO2 was monitored by the polarographic method. Intravenous injection of phenylephrine hydrochloride or trimethaphan camsylate was used to test for autoregulation by increasing or decreasing perfusion pressure. The data was analyzed in the range between 50 and 140 mmHg of mean arterial blood pressure (MABP). The range of autoregulation was determined by our own analytical method. PaCO2 was manipulated between 18.3 and 63.2 mmHg. It was increased by raising the concentration of CO2 in the inspired gas mixture. Hypocapnia was induced by hyperventilation. The mean values of CoBF and bPO2 were 36.2 +/- 5.3 ml/100 g/min and 32.9 +/- 12.8 mmHg respectively at 90 mmHg of MABP during the test for autoregulation. The changes in both CoBF and bPO2 with changing perfusion pressure were often relatively small at near baseline blood pressure and became more pronounced with large increase or decrease in MABP. On returning from high MABP to baseline blood pressure, a hysteresis effect on CoBF was observed in 20 out of twenty two cases. The autoregulation of CoBF was maintained in the range between 80 and 100 mmHg of MABP. On the other hand, bPO2 was maintained constant in the range between 75 and 110 mmHg of MABP.(ABSTRACT TRUNCATED AT 250 WORDS)     

Critical closing pressure in preterm neonates: Towards a comprehensive model of cerebral autoregulation

Abstract

In preterm neonates, intraventricular haemorrhage is linked to the dysfunction oi cerebral autoregulation (AR). We aimed at tracing the critical closing pressure (CCP) in order to quantify AR and to reveal its inner workings. In an observational study, 10 preterm neonates (median, range: ga 28 weeks, 25 to 32 weeks; bw 1070, 685 to 1730 g; age 2d, 1 to 7 d) were continuously Doppler traced (a. carotis internaj for >10min. Systemic blood pressure (BP, a. umbilicalis, a. radialis, a. temporalis) was recorded simultaneously (>1200 cardiac cycles each). Systolic BP was on average 11 mmHg above CCP. There was a striking parallel between both variables, even in cases of sudden spontaneous BP fluctuations >30% (r=0.72, 0.41 to 0.99), while systolic cerebral blood flow velocity remained largely unaffected (r=-0.15, -0.75 to 0.53), indicating a properly functioning AR. CCP was 28 mmHg 14 to 38 mmHg. Based on our data, a physiological model of AR is developed, integrating anatomy, metabolic and neuronal pathways with former physiologic findings - including low frequency cycling of cerebral blood flow velocity. Tracing of CCP is thought to have the potential to identify infants with impaired AR. Since this method is noninvasive and independent of angle of insonation (thus rendering it uncritical in probe fixation), it is a promising tool for sustained monitoring of cerebral haemadynamics in the clinical setting. [Neurol Res 1995; 17: 149–155]     

Acute hypercarbia increases the lower limit of cerebral blood flow autoregulation in a porcine model

Objectives: In the present study, our objective was to determine if hypercarbia would alter cerebral blood flow (CBF) autoregulation and reduce the ability of cerebrovascular reactivity monitoring to identify the lower limit of cerebrovascular autoregulation (LLA).

Methods: Anaesthetised juvenile pigs were assigned between two groups: normocarbia (control group, n?=?10) or hypercarbia [high carbon dioxide (CO₂) group, n?=?8]. Normocarbia subjects were maintained with an arterial CO₂ of 40?Torr, while the hypercarbia subjects had an increase of inspired CO₂ to achieve an arterial pCO₂ of >80?Torr. Gradual hypotension was induced by continuous haemorrhage from a catheter in the femoral vein, and the LLA was determined by monitoring cortical laser Doppler flux (LDF). Vascular reactivity monitoring was performed using the pressure reactivity index (PRx) and haemoglobin volume index (HVx).

Results: There were no sustained differences in ICP between groups. Autoregulation was present in both groups, despite elevation in pCO₂.The control group had an average LLA of 45?mmHg (95% CI: 43–47?mmHg) and the high CO₂ group had a LLA of 75?mmHg (95% CI: 73–77?mmHg). The detected LLA for each subject correlated with the level of pCO₂ (spearman R?=?0.8243, P?<?0.0001). Both the PRx and HVx accurately detected the LLA despite the presence of hypercarbia.

Discussion: Hypercarbia without acidosis increases the observed LLA independent of alterations in ICP. Elevations in CO₂ can impair cerebrovascular autoregulation, but if there is a sufficient increase in blood pressure above the CO₂ altered LLA, then autoregulation persists.     

Role of nitric oxide in regulation of cerebral microvascular tone and autoregulation of cerebral blood flow in cats

The role of nitric oxide in the regulation of cerebrocortical microvascular tone and autoregulation of cerebral blood flow (CBF) was examined in 24 anesthetized cats. The local cerebral blood volume (CBV), mean transit time of blood (MTT), and CBF in the cortex were measured by our photoelectric method. CBV represents the cumulative dimensions of the cerebral microvessels. Intravenous injection of 0.35–0.7 mg/kg/minN^G-monomethyl-l-arginine (l-NMMA), an inhibitor of nitric oxide synthesis, significantly increased mean arterial blood pressure (MABP; 8.4–14.1%,P < 0.01), decreased CBV (15.2–28.7%,P < 0.01), and decreased CBF (20.0–29.8%,P < 0.01) in a dose-related manner. The changes in MABP, CBV, and CBF elicited byl-NMMA were inhibited (P < 0.05) by simultaneous infusion of 35 mg/kg/minl-arginine. Autoregulation of CBF was examined during controlled hypotension of −30 to −40 mmHg (artificial bleeding) and recovery of blood pressure (reinfusion of blood). Although CBF remained constant with blood pressure changes in the control state (ΔCBF/ΔMABP of 0.037±0.155 with hypotension), CBF became dependent on blood pressure changes (ΔCBF/ΔMABP of 0.478±0.135, P < 0.05) during infusion of 0.35 mg/kg/minl-NMMA. It is concluded that nitric oxide participates in both the regulation of basal tone of cerebral microvessels and the autoregulation of CBF.     

Carotid compression: investigation of cerebral autoregulative reserve in rats

Easy-to-perform, reversible techniques to analyse cerebral autoregulation are still missing in animal research. The carotid compression technique has been established to investigate dynamic cerebral autoregulation in humans. Adapting the carotid compression technique, we compared data from the new application with that of a classical exsanguination method. Compressing the ipsilateral carotid artery with a non-traumatic clip device for 10s modulated cerebral perfusion pressure. After clip release, the peaking laser-Doppler flow velocity increase over the somatosensory cortex allowed calculation of the transient hyperaemic response ratio (THRR) in relation to baseline. Modulating blood-pressure levels maintenance of cerebral blood-flow velocity was compared with THRR responses. With decreasing blood-pressure levels, the THRR first increased (29+/-16% at 95+/-10 mmHg to 39+/-13% at 75+/-10 mmHg) before it returned to baseline values at 54+/-10 mmHg (27+/-14%). THRR significantly dropped to 11+/-12% at 34+/-11 mmHg when resting cerebral blood-flow velocity levels also started to decline. Based on the close correlation between blood-flow velocity levels and THRR responses, we have concluded that carotid compression is an alternative technique that can be used to assess cerebral autoregulation in rats. The technique allows less invasive and reversible testing of dynamic autoregulation to be performed, and the technique can easily be applied in conjunction with functional tests to potentially allow deeper insights into cerebral vasoregulative mechanisms.     

Transcranial Doppler assessment of the lower cerebral autoregulatory threshold

Continuous transcranial Doppler ultrasonography of the middle cerebral artery (TCD-MCA) has been proposed as a method of identifying the lower cerebral autoregulatory threshold. This study investigated the relationship between continuous TCD-MCA and cerebral blood flow (CBF) in sheep. Arterial blood pressure, intracranial pressure, CBF and left TCD-MCA were measured in 12 anaesthetized and ventilated merino sheep. Cerebral perfusion pressure (CPP) was reduced by haemorrhagic hypotension. Measurements were recorded continuously and breakpoint thresholds calculated by an analysis of variance. The TCD-MCA systolic velocity breakpoint (50 +/- 1.5 mmHg) did not significantly differ from the lower limit of autoregulation, identified by the CBF breakpoint (50 +/- 1.8 mmHg). The TCD-MCA diastolic velocity breakpoint occurred at a significantly higher level of CPP (64 +/- 2 mmHg) (P < 0.01). The relationship between TCD-MCA flow velocity and CBF thresholds has been described. Early divergence of flow velocity may represent a compensatory mechanism to maintain CBF.