脑血流自动调节范围内维持脑血流恒定的因素

目的探讨脑血流自动调节范围内稳定脑血流速度的血流动力学因素。方法利用经颅多普勒检测SD大鼠大脑中动脉的血流速度(cerebral blood flow velocity,CBFV),并同步记录有创动脉血压,绘制自动调节曲线,判断脑血流自动调节上、下限。计算临界关闭压(critical closing pressure,CCP)和血管面积阻力指数(resistance area product,RAP)。分析CCP、RAP与平均动脉压(mean artery blood pressure,MABP)之间的关系。结果动脉血压升高或降低过程中,正常大鼠脑血流自动调节上、下限分别为148.12±7.49 mm Hg、62.96±3.34 mm Hg。脑血流自动调节范围内,CBFV随动脉血压改变轻微(每10 mm Hg MABP,升压:0.65±0.27 cm/s;降压:0.43±0.23 cm/s),而CCP和RAP则随动脉血压明显改变(每10 mm Hg MABP,升压:4.60±1.06 mm Hg、0.11±0.04mm Hg;降压:6.74±0.59 mm Hg、0.09±0.02 mm Hg)。虽然CBFV、CCP、RAP的变化都与MABP相关,但控制CBFV的变动后,CCP和RAP随MABP改变相关性更加明显,其中CCP的变化幅度以及与MABP的相关性明显大于RAP(升压:Beta=0.561、0.418;降压:Beta=0.694、0.266,P均=0.000)。结论大鼠脑血流自动调节有效范围内,脑血流的稳定主要通过CCP和RAP改变对抗动脉血压的变动而实现,尤其是CCP相应升高或降低。     

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。     

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。     

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。     

实验性高血压对脑血流自动调节功能影响的动态观察

目的　动态观察高血压对脑血流自动调节下限的影响 ,及其与脑血管病理形态改变的关系。方法　选用 80只易卒中型肾血管性高血压大鼠 (RHRSP) ,在术后不同的时间点 ,利用临界关闭压测定脑血流自动调节下限 (LLCA) ,并动脉插管测定血压和定量分析脑血管的形态变化 ,分别与正常血压对照组 (80只 )的结果进行比较。结果　RHRSP组的LLCA术后第 6周开始升高 ,第 10周后明显高于对照组 (P <0 0 5 ) ,基本稳定于 110mmHg左右。多元回归分析发现 ,LLCA的升高主要与平均动脉压呈正相关 (r=0 96 8,P <0 0 5 ) ,与脑内微动脉的中膜厚度呈正相关 (r=0 94 0 ,P <0 0 5 )。并且LLCA的变化在平均动脉压改变的中间过程最明显 ,而于平均动脉压轻度和重度升高时变化不大 ,呈“S”形改变 (R2 =0 970 1,P <0 0 5 )。结论　高血压LLCA上移主要与平均动脉压有关 ,是脑内微动脉中膜增厚的体现 ,于血压升高中期改变最为明显。     

脑血流自动调节功能的临界关闭压测定

目的探讨测定脑血流自动调节下限(LLCA)的新方法,为LLCA的广泛临床测定奠定基础。方法同步监测正常健康志愿者正常呼吸、屏气和过度换气时的大脑中动脉血流、桡动脉血压和呼气终末呼出气体CO2分压(ETco2),然后离线计算临界关闭压(CCP)和LLCA。结果正常呼吸情况下LLCA为(58.42±10.40)mmHg,屏气时LLCA明显上升(P<0.05),过度换气时明显下降(P<0.05),且都和正常呼吸时的结果高度相关(r=0.6740、0.6429,P<0.05)。与正常呼吸相比,屏气和过度换气时LLCA测定差异的95%CI分别为(8.28￣13.68)mmHg和(-16.56￣-12.20)mmHg。屏气和过度换气时LLCA的变化率与CCP的变化率均呈负相关(r=-0.6105、-0.5551,P<0.05)。结论利用CCP可准确无创地测定人类LLCA。     

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.     

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。     

高血压对脑血流的影响及脑动脉粥样硬化的降压治疗

本期所发表的3篇有关血压管理的文章,分别讨论了高龄老年(≥80岁)高血压患者的血压管理、卒中患者的血压管理以及如何通过高质量的降压治疗预防卒中。3篇文章讨论问题的角度明显不同,但问题的核心都是如何提高高风险高血压患者降压治疗的质量,降低卒中风险,最大限度地发挥降压治疗这一最有效的预防卒中的心血管药物治疗手段的作用。对于收缩压≥160mmHg的80岁以上的高血压患者,将其血压降低到150/80mmHg,可以显著降低心脑血管并发症的风险,进一步延长这些耄耋老人的生存时间;但对于收缩压<160mmHg高血压患者,或将其血压降低到比150/80mmHg更低的水平,是否有益?仍有待进一步研究。降压治疗是预防卒中的最重要手段,但在已经有明显的脑动脉粥样硬化的患者或脑血流自动调节功能受损的患者,降压治疗有导致脑血流灌注减少的风险。这些问题都充分显示了在高风险高血压患者中血压管理的复杂性,需要更加关注降压治疗的质量。准确地测量血压,密切监测血压的变化,直接观察血管的结构与功能,如果方法可靠,测量脑血流自动调节的下限,选择起效和缓、作用时间长、一次服药能够有效控制24h血压、又具有抗动脉硬化与动脉粥样硬化作用的降压药物,以期有效、平稳地把血压控制到达标甚至理想水平,尽最大可能避免大幅度的血压波动引起的不良事件,将会给广大高风险高血压患者带来更多的益处。     

脑血流自动调节下限的无创测定方法研究

目的探讨脑血流自动调节下限(LLCA)的无创测定方法。方法选择青年健康志愿者32人,用经颅超声多普勒仪、无创血压监测仪监测和记录大脑中动脉的血流流速、桡动脉血压,用常规法和傅立叶变换法分别测定两组临界关闭压(CCP)和LLCA值。结果用常规法测定CCP有4例为负值,这4例经傅立叶变换法测定均为正值。常规法测定的LLCA值为(66.76±9.14)mmHg,傅立叶变换法测定的LLCA值为(60.79±10.12)mmHg,两者比较有显著性差异。结论临床无创测定LLCA宜用傅立叶变换法。     

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。      

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.     

Cerebral autoregulation in patients with obstructive sleep apnea syndrome during wakefulness

Background and purpose:  Obstructive sleep apnea syndrome (OSAS) is an independent risk factor for stroke. Impairment of cerebral autoregulation may play a potential role in the pre-disposition to stroke of OSAS patients. In this study, we aimed to assess dynamic cerebral autoregulation (DCA) during wakefulness in OSAS patients and a group of matched controls.
Methods:  Patients and controls were examined in the morning after an overnight complete polysomnography. Mean cerebral blood flow velocity (CBFV) in the middle cerebral artery and mean arterial blood pressure (ABP) were continuously recorded using transcranial Doppler and Finapres. DCA was assessed using the Mx autoregulatory index. Mx is a moving correlation coefficient between mean CBFV and mean ABP. More positive value of Mx indicates worse autoregulation.
Results:  Eleven OSAS patients (mean age ± SD; 52.6 ± 7.9) and 9 controls (mean age ± SD; 49.1 ± 5.3) were enrolled. The mean apnea–hypopnea index (AHI) in the OSAS group was of 22.7 ± 11.6. No significant difference was found between the two groups as for age, body mass index, mean ABP and endtidal CO₂ pressure. Cerebral autoregulation was impaired in OSAS patients compared with controls (Mx index: 0.414 ± 0.138 vs. 0.233 ± 0.100; P  = 0.009). The severity of autoregulation impairment correlated to the severity of the sleep respiratory disturbance measured by the AHI ( P  = 0.003).
Conclusion:  Cerebral autoregulation is impaired in patients with OSAS during wakefulness. Impairment of cerebral autoregulation is correlated with the severity of OSAS.     

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)     

右向左分流患者的脑血流自动调节受损:偏头痛和隐源性卒中的潜在机制

目的右向左分流(right-to-left shunts,RLS)与偏头痛和隐源性卒中之间的关系目前尚未明确。动态脑血流自动调节(dynamic cerebral autoregulation,d CA)受损可能在偏头痛和隐源性卒中的发生发展过程中起着重要的作用,本研究旨在探讨RLS是否与d CA受损有关。方法本研究共纳入66例偏头痛患者,其中36例无RLS,30例有RLS。采用经颅多普勒超声连续监测患者的脑血流速度,同时采用无创手指血压连续监测仪实时同步监测动脉血压。利用传递函数分析得出以下脑血流自动调节参数:增益、相位差(phase difference,PD)和自动调节指数(autoregulation index,ARI)。结果 RLS组偏头痛患者的PD为50.6°±22.9°,明显低于无RLS组(67.2°±18.2°,P0.001)。大量分流组的PD(45.4°±22.6°)明显低于少量分流组(64.9°±17.1°,P0.01)和无RLS组(P0.001);然而,少量分流组与无RLS组的PD值差异无显著性。RLS固有分流组的PD值(48.8°±19.9°)与潜在分流组(52.6°±26.1°)差异无显著性,但都明显低于无RLS组(P0.05)。ARI结果与PD一致。结论伴有大量RLS的偏头痛患者d CA受损,这也许是联系RLS、偏头痛和隐源性卒中的潜在机制。     

瓦氏动作在脑血流自动调节功能中的应用

CA是指脑血流在动脉血压和脑灌注压发生改变时保持相对稳定的一个复杂的多因素过 程。脑血流自动调节与多种神经系统疾病如脑血管病、帕金森病、头痛、自主神经功能障碍等疾病的 发生、发展及临床预后相关。对脑血流自动调节功能有很多种评估测量方法，监测瓦氏动作所诱导 的血压变化更具有操作性及标准化，适用于各种人群，其安全、简单、准确的特点使其在脑血流自动 调节中运用十分广泛。本文重点对瓦氏动作在脑血流自动调节功能中的应用做一个综述介绍。     

丁苯酞注射液对急性大面积脑梗死体积及基质金属蛋白酶-9的影响

目的 研究丁苯酞注射液对急性大面积脑梗死体积及血清基质金属蛋白酶- 9（m a t r i x metalloproteinases-9,MMP-9）水平的影响。 方法 将58例急性大面积脑梗死患者随机分为对照组和治疗组各29例,对照组予以脑梗死常规治 疗,治疗组在常规治疗基础上加用丁苯酞注射液。两组患者分别在入院时、入院3 d和10 d行头颅磁 共振成像（magnetic resonance imaging,MRI）,测量脑梗死体积,分别在发病12 h、48 h、72 h检测血清 MMP-9的水平。 结果 与对照组相比,治疗组入院3 d [（144.09±29.41）cm3 vs（170.21±33.09）cm3]及10 d （[ 116.57±25.73）cm3 vs（140.21±29.48）cm3]脑梗死体积缩小,差异有统计学意义。与对照组相比, 治疗组发病后48 h（[ 212.69±10.51）ng/ml vs（247.79±8.25）ng/ml）]及72 h（[ 86.14±4.84）ng/ml vs （106.10±7.03）ng/ml] MMP-9水平下降,差异有统计学意义。 结论 丁苯酞注射液可以降低急性期大面积脑梗死患者MMP-9的表达,缩小脑梗死体积。