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。     

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。     

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。     

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。     

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。     

TCD对脑血流自动调节功能的检测

脑血流自动调节是机体的一种适应能力,即灌注压变化时机体仍能保持恒定的脑血流供应。脑血流量和脑有效灌注压(CCP)成正比,与脑血管阻力(CVR)成反比,其关系为CBF=CPP/CVR。脑血流量特别是脑不同部位区域性血流量的调节,大多是通过改变脑血管阻力来完成的。在总脑血管阻力中,毛细小动     

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.     

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].     

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。     

Critical closing pressure in cerebrovascular circulation

OBJECTIVE: Cerebral critical closing pressure (CCP) has been defined as an arterial pressure threshold below which arterial vessels collapse. Hypothetically this is equal to intracranial pressure (ICP) plus the contribution from the active tone of cerebral arterial smooth muscle. The correlation of CCP with ICP, cerebral autoregulation, and other clinical and haemodynamic modalities in patients with head injury was evaluated. METHOD: intracranial pressure, arterial blood pressure (ABP) and middle cerebral artery blood flow velocity were recorded daily in ventilated patients. Waveforms were processed to calculate CCP, the transcranial Doppler-derived cerebral autoregulation index (Mx), mean arterial pressure (ABP), intracranial pressure (ICP), and cerebral perfusion pressure (CPP). RESULTS: Critical closing pressure reflected the time related changes in ICP during plateau and B waves. Overall correlation between CCP and ICP was mild but significant (R=0.41; p<0.0002). The mean difference between ABP and CCP correlated with CPP (R=0.57, 95% confidence interval (95% CI) for prediction 25 mm Hg). The difference between CCP and ICP, described previously as proportional to arterial wall tension, correlated with the index of cerebral autoregulation Mx (p<0.0002) and CPP (p<0.0001). However, by contrast with the Mx index, CCP-ICP was not significantly correlated with outcome after head injury. CONCLUSION: Critical closing pressure, although sensitive to variations in ICP and CPP, cannot be used as an accurate estimator of these modalities with acceptable confidence intervals. The difference CCP-ICP significantly correlates with cerebral autoregulation, but it lacks the power to predict outcome after head injury.     

Influence of antihypertensive treatment with budralazine on autoregulation of cerebral blood flow in spontaneously hypertensive rats

We studied the effect of chronic antihypertensive treatment with budralazine on the lower blood pressure limit of cerebral blood flow autoregulation using spontaneously hypertensive rats. Cerebral blood flow in the parietal cortex and caudate nucleus was measured to determine the lower limit using the hydrogen clearance method. The lower limit in both cerebral regions was significantly higher in 10 untreated spontaneously hypertensive rats than in 10 Wistar-Kyoto rats. The upward-shifted lower limit was restored to close to normal in the caudate nucleus and was partially restored in the parietal cortex of nine rats by 9 weeks of treatment with the high dose (50-68 mg/kg/day) of budralazine, which kept blood pressure constant at approximately normotension during the treatment period; the lower limit was slightly restored in both cerebral regions of seven rats by 4 weeks of treatment with the high dose. However, 9 weeks of treatment with the low dose (19-27 mg/kg/day) of budralazine, which produced moderate continuous hypotension in nine rats, did not apparently influence the lower limit. Our results suggest that long-term antihypertensive therapy with budralazine reduces the upward-shifted lower blood pressure limit of cerebral blood flow autoregulation toward normal and that the restoration induced by budralazine depends on the degree of blood pressure reduction as well as on the duration of the therapeutic period.     

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。      

Chronically impaired autoregulation of cerebral blood flow in long-term diabetics.

Using the arteriovenous oxygen difference method autoregulation of cerebral blood flow (CBF) was tested in 16 long-term diabetics and eight control patients. Blood pressure was raised by angiotensin infusion and lowered by trimethaphan camsylate infusion, in some cases combined with head-up tilting of the patient. Regression analysis was carried out on the results in order to quantify autoregulatory capacity. In the control patients CBF did not vary with moderate blood pressure variations, indicating normal autoregulation. In four of the 16 diabetic patients CBF showed significant pressure dependency, indicating impaired autoregulation. The cause of impaired autoregulation in some long-term diabetics is believed to be diffuse or multifocal dysfunction of cerebral arterioles due to diabetic vascular disease. Other conditions with impaired autoregulation are discussed and compared with that seen in long-term diabetes.     

Raised intracranial pressure and cerebral blood flow: 2. Supratentorial and infratentorial mass lesions in primates

Changes in cerebral blood flow with increasing intracranial pressure were studied in anaesthetized baboons during expansion of a subdural balloon in one of two different sites. With an infratentorial balloon, cerebral blood flow bore no clear relation to intracranial pressure, but was linearly related to cerebral perfusion pressure. Apart from an initial change in some animals, cerebrovascular resistance remained constant with increasing intracranial pressure, and autoregulation appeared to be lost from the outset. With a supratentorial balloon, cerebral blood flow remained constant as intracranial pressure was increased to levels around 60 mm Hg, corresponding to a cerebral perfusion pressure range of approximately 100 to 40 mmHg. Cerebrovascular resistance fell progressively, and autoregulation appeared to be effective during this phase. At higher intracranial pressure levels (lower cerebral perfusion pressure levels), autoregulation was lost and cerebral blood flow became directly dependent on cerebral perfusion pressure. The importance of the cause of the increase in intracranial pressure on the response of the cerebral circulation and the relevance of these findings to the clinical situation are discussed.     

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.     

Impairment of cerebrovascular autoregulation by theophylline

The relationship between pressure and flow was investigated in the cerebral vascular bed during intraarterial theophylline infusion. The experiments were performed on isolated canine brains supported by a donor system, thus eliminating all secondary effects of theophylline on cerebral blood flow (i.e., changes in systemic blood pressure, respiration and extracranial blood flow). Cerebral blood flow was measured continuously as the total venous outflow of the confluence of sinuses and perfusion pressure was measured in the circle of Willis. Cerebral autoregulation was tested by varying the perfusion pressure in sudden steps. The position and shape of the pressure-flow curve during theophylline infusion differed significantly from control. Theophylline induced vasodilation and a considerable impairment of cerebral autoregulation, i.e., the independence of flow and pressure over the physiological range was lost. At a perfusion pressure of 80 mm Hg the mean decrease of cerebral resistance due to theophylline was 28%. During theophylline infusion the pressure-flow regression line of the pressure range, where control flow values remained constant, differed significantly from control regression line. Possible mechanisms of cerebral vasodilation due to theophylline are discussed with regard to the impairement of cerebral autoregulation. The ability of the brain to autoregulate therefore seems dependent upon the initial degree of vasodilation due to the myotropic action of theophylline. Metabolic effects of theophylline are probably not responsible for the impairment of cerebral autoregulation.