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。     

Raised intracranial pressure and cerebral blood flow: I. Cisterna magna infusion in primates

Changes in cerebral blood flow during incremental increases of intracranial pressure produced by infusion of fluid into the cisterna magna were studied in anaesthetized baboons. Cerebral blood flow remained constant at intracranial pressure levels up to approximately 50 mm Hg. At intracranial pressure levels between 50-96 mm Hg a marked increase in cerebral blood flow occurred, associated with the development of systemic hypertension and changes in cerebrovascular resistance. Further increases of intracranial pressure led to a progressive fall in cerebral blood flow. Prior section of the cervical cord prevented both the increase in cerebral blood flow and the systemic hypertension. Alteration of cerebral perfusion pressure by bleeding during the hyperaemia in a further group of animals suggested that autoregulation was at least partially preserved during this phase. After maximum hyperaemia had occurred, however, autoregulation appeared to be lost. The clinical implications of these findings are discussed.     

Cerebral autoregulation in middle cerebral artery territory precedes that of posterior cerebral artery in human cortex.

OBJECTIVE: Cerebral autoregulation tends to compensate changes in arterial blood pressure. This mechanism of cerebral blood flow regulation appears to be insufficient in orthostatic dysregulation in which mainly vertebrobasilar symptoms occur. To investigate this hypothesis, we compared cerebral autoregulation in the vascular territory of the carotic and vertebrobasilar vessel system using a leg cuff test to induce a drop in cerebral perfusion pressure. METHODS: We measured blood flow velocity in 10 healthy young volunteers (aged 26.7 +/- 0.3 years, 7 male) simultaneously in the middle and posterior cerebral artery with transcranial Doppler sonography. A leg cuff test was used to induce a sudden decrease in arterial blood pressure. Arterial blood pressure was measured with a non-invasive photoplethysmographic method. The averaged relative blood flow velocity changes due to the pressure step were compared between both vessel territories. RESULTS: After cuff release systolic (diastolic) blood flow velocity increased with a latency of 1.1 +/- 0.3 s (1.8 +/- 0.4 s). Due to a smaller decrease and identical time courses cerebral blood flow velocity recovery in the posterior cerebral artery precedes blood flow recovery in the middle cerebral artery by 0.9 +/- 0.3 s. DISCUSSION: Cerebral autoregulation in the carotid and vertebrobasilar system does not differ in the time course of the blood flow velocity recovery. Due to a smaller decrease in blood flow velocity recovery in the posterior cerebral artery precedes recovery in the middle cerebral artery by nearly 1 s.     

Continuous monitoring of cerebrovascular autoregulation: a validation study

BACKGROUND: Continuous monitoring of dynamic cerebral autoregulation, using a moving correlation index of cerebral perfusion pressure and mean middle cerebral artery flow velocity, may be useful in patients with severe traumatic brain injury to guide treatment, and has been shown to be of prognostic value. OBJECTIVE: To compare an index of dynamic cerebral autoregulation (Mx) with an index of static cerebral autoregulation (sRoR). METHODS: Mx was validated in a prospective comparative study against sRoR, using 83 testing sessions in 17 patients with traumatic brain injury. sRoR and Mx were calculated simultaneously during pharmacologically induced blood pressure variations. RESULTS: Mx was significantly correlated with sRoR (R = -0.78, p < 0.05). Nine patients were found to have failure of cerebral autoregulation, with an sRoR value < 50%. If an Mx value of 0.3 was used as the cut off point for failure of cerebral autoregulation, this index had 100% sensitivity and 90% specificity for demonstrating failure of autoregulation compared with the sRoR. An increase in cerebral blood flow velocity correlated significantly with Mx (R = 0.73, p < 0.05) but not with cerebral perfusion pressure (R = 0.41). CONCLUSIONS: Dynamic and static cerebral autoregulation are significantly correlated in traumatic brain injury. Cerebral autoregulation can be monitored continuously, graded, and reliably assessed using a moving correlation analysis of cerebral perfusion pressure and cerebral blood flow velocity (Mx). The Mx index can be used to monitor cerebral blood flow regulation. It is useful in traumatic brain injury because it does not require any external stimulus.     

Hemodynamic effect of carotid endarterectomy

Cerebral blood flow was measured by the intravenous xenon-133 technique at rest and during cerebral vasodilation with acetazolamide in 32 patients before and after uncomplicated carotid endarterectomy. The results were compared with the internal carotid artery perfusion pressure measured during surgery. A significant improvement in side-to-side cerebral blood flow asymmetry occurred in 6 patients studied at baseline and in 11 patients during provoked cerebral vasodilation. These patients all belonged to a group of 14 patients who, in addition to a severe stenosis of the internal carotid artery, presented a reduction in cerebral perfusion pressure of at least 20%. No improvements occurred in 18 patients with no or only minor reduction in perfusion pressure, irrespective of the degree of stenosis. These findings indicate an improved perfusion reserve following carotid endarterectomy in most patients with marked reduction in perfusion pressure, whereas only some of these patients will experience an improvement in baseline cerebral blood flow.     

Cerebral vasomotor reactivity testing in head injury: the link between pressure and flow

BACKGROUND: It has been suggested that a moving correlation index between mean arterial blood pressure and intracranial pressure, called PRx, can be used to monitor and quantify cerebral vasomotor reactivity in patients with head injury. OBJECTIVES: To validate this index and study its relation with cerebral blood flow velocity and cerebral autoregulation; and to identify variables associated with impairment or preservation of cerebral vasomotor reactivity. METHODS: The PRx was validated in a prospective study of 40 head injured patients. A PRx value of less than 0.3 indicates intact cerebral vasomotor reactivity, and a value of more than 0.3, impaired reactivity. Arterial blood pressure, intracranial pressure, mean cerebral perfusion pressure, and cerebral blood flow velocity, measured bilaterally with transcranial Doppler ultrasound, were recorded. Dynamic cerebrovascular autoregulation was measured using a moving correlation coefficient between arterial blood pressure and cerebral blood flow velocity, the Mx, for each cerebral hemisphere. All variables were compared in patients with intact and impaired cerebral vasomotor reactivity. RESULTS: No correlation between arterial blood pressure or cerebral perfusion pressure and cerebral blood flow velocity was seen in 19 patients with intact cerebral vasomotor reactivity. In contrast, the correlation between these variables was significant in 21 patients with impaired cerebral vasomotor reactivity, whose cerebral autoregulation was reduced. There was no correlation with intracranial pressure, arterial blood pressure, cerebral perfusion pressure, or interhemispheric cerebral autoregulation differences, but the values for these indices were largely within normal limits. CONCLUSIONS: The PRx is valid for monitoring and quantifying cerebral vasomotor reactivity in patients with head injury. This intracranial pressure based index reflects changes in cerebral blood flow and cerebral autoregulatory capacity, suggesting a close link between blood flow and intracranial pressure in head injured patients. This explains why increases in arterial blood pressure and cerebral perfusion pressure may be useful for reducing intracranial pressure in selected head injured patients (those with intact cerebral vasomotor reactivity).     

Preservation of cerebral autoregulation in the unanesthetized hypoxemic newborn dog

Studies were conducted to determine the effects of hypoxemia on cerebral blood flow and the influence of hyperoxia and hypoxemia on autoregulation of cerebral blood flow in the unanesthetized newborn dog. Twenty-one newborn dogs less than 2 weeks of age were studied. Cerebral blood flow was measured using radioactive microspheres during successive periods of normotension, hypotension (produced by blood withdrawal) and normotension (produced by infusion of previously withdrawn blood). In the hyperoxic animals, arterial pO2 was maintained above 250 torr by having the animal breathe 100% oxygen, while in the hypoxemic animals arterial pO2 was maintained between 30 and 35 torr by having the animal breathe 12% O2. Cerebral blood flow increased significantly with hypoxemia. In both hypoxemic and hyperoxic animals cerebral blood flow was maintained constant in spite of a large fall in arterial blood pressure and cardiac output, demonstrating the presence of autoregulation. Calculated oxygen transport to the brain was constant during hypoxemia and hypotension in all animals. Thus autoregulation of cerebral blood flow is present in newborn animals and is preserved under conditions of moderate hypoxemia.     

Effect of epoprostenol (prostacyclin, PGI2) on cerebral blood flow in man.

Cerebral blood flow has been measured using the non-invasive Xenon133 clearance technique in eight normal subjects during an infusion of epoprostenol (prostacyclin, PGI2) at a dose of 5 ng/kg/min. The results were compared with a control infusion of saline given in a balanced order. PGI2 was found to result in a reduction in cerebral blood flow of about 8%. PGI2 also caused a small drop in diastolic blood pressure and it is proposed that the fall in cerebral blood flow may have been the result of disturbed autoregulation. The findings suggest that the therapeutic use of PGI2 in patients with cerebral artery spasm would not be accompanied by undesirable intracerebral steal.     

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.     

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。     

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。     

Cerebral autoregulation in Alzheimer's disease

Cerebral autoregulation aims to stabilize blood flow to the brain during variations in perfusion pressure, thus protecting the brain against the risks of low or high systemic blood pressure. This vital mechanism is severely impaired in the transgenic mouse model of Alzheimer''s disease (AD) that abundantly produces amyloid-β peptide β₁₋₄₂. These observations have been extrapolated to human AD, wherein impairment of autoregulation could have important implications for the clinical management and prevention of AD. Research on cerebral autoregulation in human AD, however, has only recently become available. Contrary to the animal models, preliminary studies suggest that cerebral autoregulation is preserved in patients with AD. Further research is urgently needed to elucidate this discrepancy in the current literature, given the accumulating evidence that implicates cerebrovascular pathology in AD.     

Critical limits of pressure-flow relation in the human brain.

BACKGROUND: This study was designed to determine the minimal mean flow velocity and pressure-flow relation necessary to preserve human consciousness. METHODS: Passive upright tilt provocation was used in conjunction with transcranial Doppler in 80 patients with a history of syncope of unknown etiology. Cerebral blood flow velocity, blood pressure, and heart rate were monitored noninvasively. RESULTS: Forty patients remained asymptomatic, and the rest had clinically induced true syncope or premonitory symptoms. In the asymptomatic group, there was a 23 +/- 16% (p = 0.000) drop in mean flow velocity, but no significant changes in systolic and diastolic blood pressures. In the symptomatic patients, there was a 58 +/- 14% (p = 0.000) drop in mean flow velocity, 37 +/- 23% (p = 0.000) fall in systolic pressure, and 31 +/- 20% (p = 0.000) fall in diastolic pressure. In 80% of symptomatic patients, the critical lower limit of mean flow velocity was at -50% of resting baseline while patients were lying supine. The symptomatic group had lower mean flow velocity and blood pressure responses as compared with the asymptomatic group. The slope and intercept values of the pressure (y axis) to flow velocity (x axis) regression curves indicate a greater degree of impaired autoregulation in the symptomatic group (y = 0.529 x-6.11, r2 = 0.108, p = 0.038) as compared with the asymptomatic (y = 0.317 x + 0.966, r2 = 0.14, p = 0.017). CONCLUSIONS: The critical lower limit of cerebral perfusion lies at 50% below baseline supine mean flow velocity.     

Neurovascular Coupling and Cerebral Autoregulation in Patients with Stenosis of the Posterior Cerebral Artery

Neurovascular coupling and cerebral autoregulation are two brain intrinsic vasoregulative mechanisms that rapidly adjust local cerebral blood flow. This study examined if stenotic disease affects both mechanisms in the posterior cerebral artery. Ten patients with altogether 13 stenosed (≥50%) posterior cerebral artery (PCA) sides were studied. In addition, 6 control persons without a PCA stenosis were examined. Cerebral blood flow velocity was assessed from both PCAs with transcranial Doppler sonography; blood pressure was measured noninvasively via fingerplethysmography. Neurovascular coupling was assessed by a control system approach using a standard visual stimulation paradigm. Cerebral autoregulation dynamics were measured from spontaneous oscillations of blood pressure and cerebral blood flow velocity by transfer function analysis (phase and gain). The parameters of neurovascular coupling and cerebral autoregulation did not show relevant differences between controls, nonstenosed sides, and stenosed sides. The 3 severely stenosed PCA sides showed a trend to a minor functional flow velocity change and attenuation of the neurovascular coupling mechanism in relation to sides with moderate stenosis. Phase and gain were not altered on sides with PCA stenosis. We conclude that in a group of patients with mainly moderate stenosis of the PCA neurovascular coupling and dynamic autoregulation dynamics seem to be unaltered.     

Dynamic cerebral autoregulation in stroke patients with a central sympathetic deficit

Gierthmühlen J, Allardt A, Sawade M, Baron R, Wasner G. Dynamic cerebral autoregulation in stroke patients with a central sympathetic deficit.
Acta Neurol Scand: 2011: 123: 332–338.
© 2010 John Wiley & Sons A/S. Objective – To investigate the functional role of the sympathetic innervation on cerebral autoregulation. Materials and methods – Seventeen patients with infarction of the dorsolateral medulla oblongata affecting central sympathetic pathways (Wallenberg′s syndrome) and 21 healthy controls were included in the study. Cerebral blood flow velocity (CBFV) in the medial cerebral artery was investigated using transcranial Doppler ultrasound during decrease in cerebral perfusion pressure induced by leg‐cuff test and tilt table. Results – Upon leg‐cuff test, changes of cerebral blood flow and mean arterial blood pressure as well as autoregulatory index did not differ between patients or controls. No differences were found in changes of CBFV, mean arterial blood pressure and heart rate between patients or controls during the tilt table test. Conclusions – We suggest that the sympathetic nervous system does not have an influence on cerebral autoregulation after decrease in perfusion pressure under normotonous conditions.     

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。     

Hemodynamic significance of internal carotid artery disease

Neurologic symptoms in the region of an internal carotid artery stenosis are considered to be embolic in most instances. Only in a subgroup has carotid occlusive disease with impairment of the collateral supply, caused a state of hemodynamic failure with marked reduction of perfusion pressure. Though unproven, it is reasonable to assume that without surgical intervention, the risk is higher than average for patients with hemodynamic failure. Equally, should there be any postoperative improvement of cerebral blood flow or neurologic deficits, it should be looked for in this group. Thus, it is necessary to distinguish those with low perfusion pressure from the population of patients with carotid artery disease. Preoperative clinical evaluation and direct visualization of the carotid bifurcation should be supplemented by indirect physiological tests which allow assessment of collateral perfusion. Examination of periorbital flow direction or oculoplethysmography could be used as a screening procedure. Negative tests most certainly rule out any severe pressure gradient across the stenosis, irrespective of the luminal reduction. A positive result, on the other hand, should be further quantified since most indirect tests become positive at relatively small pressure gradients. Studies of cerebral blood flow at rest and during cerebral vasodilation makes it possible to identify patients with severe reduction of cerebral perfusion pressure. Such hemodynamic failure of one hemisphere may be identified in most cases by a conventional non-invasive xenon-133 technique and stationary detectors. Smaller focal regions of hypoperfusion may be identified by computer emission tomography, either by the detection of single-photon emission or by paired detection of annihilation photons. Endarterectomy does improve cerebral hemodynamics in terms of increased flow through the reconstructed vessel and elimination of pressure gradients. The cerebral blood flow, though remains unchanged in the majority of patients, at least when measured at baseline. Only in those patients with a reduction in perfusion pressure can a significant improvement in baseline flow occur. Flow reserve determined by cerebral vasodilation, however, will improve in most patients with hemodynamic failure. In addition, some patients in the low-pressure group develop marked, but temporary, hyperperfusion after reconstruction of very high grade carotid stenosis. This is considered a result of chronic low perfusion pressure with subsequent loss of autoregulation, and autoregulatory control is first regained after some days.(ABSTRACT TRUNCATED AT 400 WORDS)     

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.     

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.     

Cardiovascular and cerebrovascular responses to lower body negative pressure in type 2 diabetic patients

In diabetic patients, vascular disease and autonomic dysfunction might compromise cerebral autoregulation and contribute to orthostatic intolerance. The aim of our study was to determine whether impaired cerebral autoregulation contributes to orthostatic intolerance during lower body negative pressure in diabetic patients. Thirteen patients with early-stage type 2 diabetes were studied. We continuously recorded RR-interval, mean blood pressure and mean middle cerebral artery blood flow velocity at rest and during lower body negative pressure applied at -20 and -40 mm Hg. Spectral powers of RR-interval, blood pressure and cerebral blood flow velocity were analyzed in the sympathetically mediated low (LF: 0.04-0.15 Hz) and the high (HF: 0.15-0.5 Hz) frequency ranges. Cerebral autoregulation was assessed from the transfer function gain and phase shift between LF oscillations of blood pressure and cerebral blood flow velocity. In the diabetic patients, lower body negative pressure decreased the RR-interval, i.e. increased heart rate, while blood pressure and cerebral blood flow velocity decreased. Transfer function gain and phase shift remained stable. Lower body negative pressure did not induce the normal increase in sympathetically mediated LF-powers of blood pressure and cerebral blood flow velocity in our patients indicating sympathetic dysfunction. The stable phase shift, however, suggests intact cerebral autoregulation. The dying back pathology in diabetic neuropathy may explain an earlier and greater impairment of peripheral vasomotor than cerebrovascular control, thus maintaining cerebral blood flow constant and protecting patients from symptoms of presyncope.