Cerebral Blood Velocity Research Articles

Effects of aging on the association between cerebrovascular responses to visual stimulation, hypercapnia and arterial stiffness

Aging is associated with decreased vascular compliance and diminished neurovascular- and hypercapnia-evoked cerebral blood flow (CBF) responses. However, the interplay between arterial stiffness and reduced CBF responses is poorly understood. It was hypothesized that increased cerebral arterial stiffness is associated with reduced evoked responses to both, a flashing checkerboard visual stimulation (i.e., neurovascular coupling), and hypercapnia. To test this hypothesis, 20 older (64 ± 8 year; mean ± SD) and 10 young (30 ± 5 year) subjects underwent a visual stimulation (VS) and a hypercapnic test. Blood velocity through the posterior (PCA) and middle cerebral (MCA) arteries was measured concurrently using transcranial Doppler ultrasound (TCD). Cerebral and systemic vascular stiffness were calculated from the cerebral blood velocity and systemic blood pressure waveforms, respectively. Cerebrovascular (MCA: young = 76 ± 15%, older = 98 ± 19%, p = 0.004; PCA: young = 80 ± 16%, older = 106 ± 17%, p < 0.001) and systemic (young = 59 ± 9% and older = 80 ± 9%, p < 0.001) augmentation indices (AI) were higher in the older group. CBF responses to VS (PCA: p < 0.026) and hypercapnia (PCA: p = 0.018; MCA: p = 0.042) were lower in the older group. A curvilinear model fitted to cerebral AI and age showed AI increases until ~60 years of age, after which the increase levels off (PCA: R2 = 0.45, p < 0.001; MCA: R2 = 0.31, p < 0.001). Finally, MCA, but not PCA, hypercapnic reactivity was inversely related to cerebral AI (MCA: R2 = 0.28, p = 0.002; PCA: R2 = 0.10, p = 0.104). A similar inverse relationship was not observed with the PCA blood flow response to VS (R2 = 0.06, p = 0.174). In conclusion, older subjects had reduced neurovascular- and hypercapnia-mediated CBF responses. Furthermore, lower hypercapnia-mediated blood flow responses through the MCA were associated with increased vascular stiffness. These findings suggest the reduced hypercapnia-evoked CBF responses through the MCA, in older individuals may be secondary to vascular stiffening.

Self-reported tolerance influences cerebral blood flow during exercise

Discussion: Our findings demonstrate, for the first time, that exercise during water immersion modifies haemodynamic variables and increases mean arterial pressure. This is associated with increased cerebral blood velocities, relative to land based exercise of a similar intensity. These novel data suggest that exercise undertaken in thewatermay decrease cerebrovascular risk. Future studies will focus on the chronic effect of exercise conducted in water on brain health and cognitive function.

Evaluation of SWI in Children with Sickle Cell Disease

SWI is a powerful tool for imaging of the cerebral venous system. The SWI venous contrast is affected by blood flow, which may be altered in sickle cell disease. In this study, we characterized SWI venous contrast in patients with sickle cell disease and healthy control participants and examined the relationships among SWI venous contrast, and hematologic variables in the group with sickle cell disease. A retrospective review of MR imaging and hematologic variables from 21 patients with sickle cell disease and age- and sex-matched healthy control participants was performed. A Frangi vesselness filter was used to quantify the attenuation of visible veins from the SWI. The normalized visible venous volume was calculated for quantitative analysis of venous vessel conspicuity. The normalized visible venous volume was significantly lower in the group with sickle cell disease vs the control group (P < .001). Normalized visible venous volume was not associated with hemoglobin, percent hemoglobin F, percent hemoglobin S, absolute reticulocyte count, or white blood cell count. A hypointense arterial signal on SWI was observed in 18 of the 21 patients with sickle cell disease and none of the 21 healthy control participants. This study demonstrates the variable and significantly lower normalized visible venous volume in patients with sickle cell disease compared with healthy control participants. Decreased venous contrast in sickle cell disease may reflect abnormal cerebral blood flow, volume, velocity, or oxygenation. Quantitative analysis of SWI contrast may be useful for investigation of cerebrovascular pathology in patients with sickle cell disease, and as a tool to monitor therapies. However, future studies are needed to elucidate physiologic mechanisms of decreased venous conspicuity in sickle cell disease.

Cerebral blood flow is governed by the capillary pumps driven by electricity of neurons and their heat and CO2 production. Hammock posture is the optimal one

to the editor: We applaud Dr. Zuj and colleagues ([5][1]) for their study describing the relative contribution of arterial CO2 partial pressure (PaCO2) and brain level arterial pressure (BPMCA) for the syncope, prior- and post-head-down bed rest (HDBR). We appreciate their conclusion that cerebral

Effects of inspiratory resistance on cerebral blood velocity during orthostasis with dehydration

Inspiratory resistance increases low frequency (LF) middle cerebral artery blood velocity (MCAv) oscillations and delays symptoms of pre‐syncope during lower body negative pressure, despite reductions in absolute MCAv. We tested the hypothesis that during central hypovolemia induced by combined dehydration and orthostasis (via head‐up tilt, HUT), inspiratory resistance would increase MCAv oscillations and attenuate pre‐syncopal symptoms. 10 subjects were tilted to 70° for 10‐min under euhydration (EUH) and dehydration (DEH; 40 mg of furosemide/fluid restriction) conditions, with and without inspiratory resistance (Impedance Threshold Device, ITD) in a randomized, cross‐over design. Arterial pressure (AP) and MCAv were measured continuously. DEH decreased blood (6.5±0.9%) and plasma (11.2±1.4%) volume (both P&lt;0.01), but did not impact AP or MCAv (P≥0.25) at rest. HUT decreased AP and MCAv under both EUH and DEH (P≤0.016) with no difference between hydration conditions (P=0.498). ITD breathing did not attenuate the fall in AP or MCAv under either hydration condition (P≥0.123), and subjective pre‐syncopal symptoms were similar across all conditions (P=0.78). ITD breathing increased MCAv LF oscillations under both hydration conditions during HUT (P≤0.05). While ITD breathing increased MCAv LF oscillations during DEH and HUT, it did not attenuate the decrease in MCAv or the reporting of symptoms.

The effects of head‐up and head‐down tilt on cerebrovascular CO2 reactivity in anterior and posterior cerebral circulations

Cerebral autoregulation is a protective feature of the cerebrovasculature that maintains relatively constant cerebral perfusion in the face of static and dynamic fluctuations in mean arterial pressure (MAP). However, gravity‐dependent shifts in blood volume distribution during head‐up and head‐down tilt (HUT, HDT) have profound effects on venous return, cardiac output and MAP. Further, cerebral blood flow (CBF) is highly sensitive to the influence of changes in arterial CO2 (PaCO2) on arteriolar diameter. We tested the effects of steady‐state tilt on cerebral blood velocity (CBV) and CO2 reactivity in the middle and posterior cerebral arteries (MCA, PCA) using hyperoxic rebreathing and transcranial Doppler ultrasound in various positions on a tilt table. Following initial testing in supine position, subjects were positioned randomly and tested in each of four positions: 90° HDT, 45° HDT, 45° HUT and 90° HUT. There were no differences in steady‐state MCA or PCA CBV across positions. Absolute and relative CO2 reactivity slopes were calculated for the MCA and PCA using linear regression. Absolute reactivity was greater in the MCA than the PCA in all 5 positions, but there was no interaction between reactivity and tilt. Our data demonstrate that CBF is maintained through cerebral autoregulation in the face of superimposed steady‐state orthostatic stress and dynamic changes in PaCO2.

The influence of combined lower body negative pressure and mental stress on cerebral blood flow in men and women

Lower body negative pressure (LBNP) decreases mean middle cerebral blood velocity (MCAv) and mental stress (MS) typically increases MCAv, but the MCAv response to these combined autonomic stressors is unknown. We hypothesized that performing MS during LBNP would result in an additive MCAv interaction. Eighteen participants (9 men, 9 women) completed three randomized trials: 1) 3 min LBNP (−40 mmHg), 2) 3 min MS (serial subtraction), and 3) combined LBNP and MS. Mean arterial pressure (MAP), heart rate (HR) and MCAv were continuously measured. Baseline MAP (81±2 vs. 80±1 vs. 80±1 mmHg) and HR (65±2 vs. 64±2 vs. 65±2 beats/min) were similar preceding each trial. LBNP significantly (p&lt;0.05) decreased MCAv (Δ−3±1 cm/s), but did not alter MAP or HR. MS significantly (p&lt;0.05) increased MAP (Δ10±1 mmHg), HR (Δ17±2 beats/min) and MCAv (Δ3±1 cm/s; p=0.05). Combined LBNP and MS significantly (P&lt;0.05) increased MAP (Δ7±3 mmHg) and HR (Δ18±4 beats/min) and significantly decreased MCAv (Δ−5±2 cm/s). Increases in MAP and HR were similar during the combination trial when compared to the calculated sum of the individual trials. However, the MCAv (Δ−5±2 vs. Δ0±2 cm/s) response was blunted during the combination trial vs. the sum of individual trials. In conclusion, our findings are contrary to our hypothesis and suggest there is not an additive MCAv interaction during combined cognitive and orthostatic stress.Supported by NASA.

Cerebral hypoperfusion modifies the respiratory chemoreflex during orthostatic stress

The respiratory chemoreflex is known to be modified during orthostatic stress although the underlying mechanisms remain to be established. To determine the potential role of cerebral hypoperfusion, we examined the relationship between changes in MCA Vmean (middle cerebral artery mean blood velocity) and V̇E (pulmonary minute ventilation) from supine control to LBNP (lower body negative pressure; −45mmHg) at different CO2 levels (0, 3.5 and 5% CO2). The regression line of the linear relationship between V̇E and PETCO2 (end-tidal CO2) shifted leftwards during orthostatic stress without any change in sensitivity (1.36±0.27 l/min per mmHg at supine to 1.06±0.21 l/min per mmHg during LBNP; P=0.087). In contrast, the relationship between MCA Vmean and PETCO2 was not shifted by LBNP-induced changes in PETCO2. However, changes in V̇E from rest to LBNP were more related to changes in MCA Vmean than changes in PETCO2. These findings demonstrate for the first time that postural reductions in CBF (cerebral blood flow) modified the central respiratory chemoreflex by moving its operating point. An orthostatically induced decrease in CBF probably attenuated the ‘washout’ of CO2 from the brain causing hyperpnoea following activation of the central chemoreflex.

Cerebral hypoperfusion modifies the respiratory chemoreflex during orthostatic stress

The respiratory chemoreflex is known to be modified during orthostatic stress although the underlying mechanisms remain to be established. To determine the potential role of cerebral hypoperfusion, we examined the relationship between changes in MCA V(mean) (middle cerebral artery mean blood velocity) and ˙VE (pulmonary minute ventilation) from supine control to LBNP (lower body negative pressure; −45mmHg) at different CO(2) levels (0, 3.5 and 5% CO(2)). The regression line of the linear relationship between ˙V(E) and PETCO(2) (end-tidal CO(2)) shifted leftwards during orthostatic stress without any change in sensitivity (1.36+− 0.27 l/min per mmHg at supine to 1.06+− 0.21 l/min per mmHg during LBNP; P=0.087). In contrast, the relationship between MCA V(mean) and PETCO(2) was not shifted by LBNP-induced changes in PETCO2. However, changes in ˙V(E) from rest to LBNP were more related to changes in MCA V(mean) than changes in PETCO(2). These findings demonstrate for the first time that postural reductions in CBF (cerebral blood flow) modified the central respiratory chemoreflex by moving its operating point. An orthostatically induced decrease in CBF probably attenuated the ‘washout’ of CO(2) from the brain causing hyperpnoea following activation of the central chemoreflex.

Transcranial Doppler Ultrasonography in Beta-thalassemia Major Patients Without and With Thrombocytosis

BackgroundBeta-thalassemia is a type of anemia in which the patients may require splenectomy and this can lead to thrombocytosis with increased risk of stroke. Transcranial Doppler ultrasound is a method for determining cerebral vessel stenosis.ObjectivesThe aim of this study was to investigate whether the risk of a future stroke secondary to cerebral artery stenosis can be predicted with the use of transcranial Doppler ultrasound in beta-thalassemia major patients.Patients and MethodsThis study included 54 beta-thalassemia major patients divided into 2 groups; group A consisted of 28 patients who have thrombocytosis secondary to a previous splenectomy and group B comprised of 26 patients who did not have a splenectomy with normal platelet count, as well as a control group of 30 healthy individuals.ResultsTranscranial Doppler ultrasound of the cerebral vessels were performed in all participants, and the results for each group were compared with the controls. In addition, patients were evaluated for evidence of high flow velocity in the cerebral vessels that met the clinically significant criteria of ≥ 50% stenosis. Transcranial Doppler ultrasound velocity criteria for > 50% stenosis, indicating a risk of stroke, were not documented in any patients but increase in cerebral blood velocities in many arteries in group A and in some arteries in group B were revealed.ConclusionFollowing splenectomy, thrombocytosis can predispose the patients to an increase in cerebral blood velocities more than respected with anemia. But by transcranial doppler ultrasonography no evidence of significant stenosis were found in intracerebral arteries to conclude that the beta-thalassemia major patients were more prone to the development of stroke secondary to this abnormality.

Serial monitoring of CO2 reactivity following sport concussion using hypocapnia and hypercapnia

Primary objective: This study examined the effects of mild traumatic brain injury (mTBI) on cerebrovascular reactivity (CVR).Research design: A repeated measures design was used to examine serial changes in CVR.Methods and procedures: Twenty subjects who recently suffered a mTBI were subjected to a respiratory challenge consisting of repeated 20 s breath-holds (BH) and hyperventilations (HV). Testing occurred on days 2 (D2), 4 (D4) and 8 (D8) post-injury as well as a baseline (BASE) assessment (after return-to-play). Transcranial Doppler was used to assess mean cerebral blood velocity (vMCA) and expired gas analysis provided end-tidal carbon dioxide (PETCO2) levels.Results: There was no significant difference in resting vMCA across all testing days for mTBI. No significant differences in PETCO2 were found throughout the testing protocol. A significant effect (p < 0.001) of testing day on vMCA was found during BH and HV challenges for mTBI. Post-hoc analysis revealed significant differences (p < 0.05) in vMCA between D2 and the other testing days.Conclusions: These data suggest that, following mTBI: (1) CVR is not impaired at rest; (2) CVR is impaired in response to respiratory stress; and (3) the impairment may be resolved as early as 4 days post-injury.

Cerebral critical closing pressure and CO2 responses during the progression toward syncope

Syncope from sustained orthostasis results from cerebral hypoperfusion associated with reductions in arterial pressure at the level of the brain (BPMCA) and reductions in arterial CO2 as reflected by end-tidal values (PetCO2). It was hypothesized that reductions in PetCO2 increase cerebrovascular tone before a drop in BPMCA that ultimately leads to syncope. Twelve men (21-42 yr of age) completed an orthostatic tolerance test consisting of head-up tilt and progressive lower body negative pressure to presyncope, before and after completing 5 days of continuous head-down bed rest (HDBR). Cerebral blood velocity (CBFV), BPMCA, and PetCO2 were continuously recorded throughout the test. Cerebrovascular indicators, cerebrovascular resistance, critical closing pressure (CrCP), and resistance area product (RAP), were calculated. Comparing from supine baseline to 6-10 min after the start of tilt, there were reductions in CBFV, PetCO2, BPMCA, and CrCP, an increase in RAP, and no change in cerebrovascular resistance index. Over the final 15 min before syncope in the pre-HDBR tests, CBFV and CrCP were significantly related to changes in PetCO2 (r = 0.69 ± 0.17 and r = 0.63 ± 0.20, respectively), and BPMCA, which was not reduced until the last minute of the test, was correlated with a reduction in RAP (r = 0.91 ± 0.09). Post-HDBR, tilt tolerance was markedly reduced, and changes in CBFV were dominated by a greater reduction in BPMCA with no relationships to PetCO2. Therefore, pre-HDBR, changes in PetCO2 with orthostasis contributed to increases in cerebrovascular tone and reductions in CBFV during the progression toward syncope, whereas, after 5 days of HDBR, orthostatic responses were dominated by changes in BPMCA.

Hemodynamic Instability Increases New Ischemic Brain Lesions on Diffusion-Weighted Imaging After Carotid Artery Stenting

Hemodynamic instability (HI) may impair the washout of debris during distal intracranial circulation and increase the risk of clinically evident cerebral ischemia. However, the interaction between HI and new ischemic brain lesions detected on diffusion-weighted imaging (DWI) has not been examined. This study evaluated whether HI was significantly associated with the incidence of new ischemic brain lesions on DWI. Data on 128 patients who underwent carotid artery stenting (CAS) with the same devices and procedures between January 2005 and May 2010 were retrospectively analyzed. HI was noted in 31 (24.2%) patients. New ischemic brain lesions were detected on DWI in 25 (19.5%) patients. Ten of 31 (32.2%) patients with HI showed new ischemic brain lesions on DWI. Fifteen of 97 (15.5%) patients without HI showed new lesions. Univariate analysis showed that patients with HI had a significantly higher incidence of new ischemic brain lesions than patients without HI (p = 0.04). A multivariable model showed that age and HI were significantly associated with the incidence of new ischemic brain lesions. In patients with carotid artery stenosis, decreased blood pressure produced no active vascular response, but reduced the cerebral blood volume and velocity due to impaired dynamic cerebral autoregulation. The results of this study suggest that HI with CAS induces impaired clearance of microembolisms and causes an increased number of new ischemic brain lesions detected on DWI.

Middle cerebral artery blood velocity during running

Running induces characteristic fluctuations in blood pressure (BP) of unknown consequence for organ blood flow. We hypothesized that running-induced BP oscillations are transferred to the cerebral vasculature. In 15 healthy volunteers, transcranial Doppler-determined middle cerebral artery (MCA) blood flow velocity, photoplethysmographic finger BP, and step frequency were measured continuously during three consecutive 5-min intervals of treadmill running at increasing running intensities. Data were analysed in the time and frequency domains. BP data for seven subjects and MCA velocity data for eight subjects, respectively, were excluded from analysis because of insufficient signal quality. Running increased mean arterial pressure and mean MCA velocity and induced rhythmic oscillations in BP and in MCA velocity corresponding to the difference between step rate and heart rate (HR) frequencies. During running, rhythmic oscillations in arterial BP induced by interference between HR and step frequency impact on cerebral blood velocity. For the exercise as a whole, average MCA velocity becomes elevated. These results suggest that running not only induces an increase in regional cerebral blood flow but also challenges cerebral autoregulation.

The clinical effectiveness and cost-effectiveness of primary stroke prevention in children with sickle cell disease: a systematic review and economic evaluation.

Sickle cell disease (SCD) is a recessive genetic blood disorder, caused by a mutation in the β-globin gene. For children with SCD, the risk of stroke is estimated to be up to 250 times higher than in the general childhood population. Transcranial Doppler (TCD) ultrasonography is a non-invasive technique which measures local blood velocity in the proximal portions of large intracranial arteries. Screening with TCD ultrasonography identifies individuals with high cerebral blood velocity; these children are at the highest risk of stroke. A number of primary stroke prevention strategies are currently used in clinical practice in the UK including blood transfusion, treatment with hydroxycarbamide and bone marrow transplantation (BMT). No reviews have yet assessed the clinical effectiveness and cost effectiveness of primary stroke prevention strategies in children with SCD identified to be at high risk of stroke using TCD ultrasonography. To assess the clinical effectiveness and cost-effectiveness of primary stroke prevention treatments for children with SCD who are identified (using TCD ultrasonography) to be at high risk of stroke. Electronic databases were searched from inception up to May 2011, including the Cochrane Database of Systematic Reviews (CDSR), the Cochrane Central Register of Controlled Trials (CENTRAL), the Database of Abstracts of Reviews of Effects (DARE), EMBASE, the Health Technology Assessment (HTA) database, ISI Web of Science Proceedings, ISI Web of Science Citation Index, the NHS Economic Evaluation Database (NHS EED) and MEDLINE. The assessment was conducted according to accepted procedures for conducting and reporting systematic reviews and economic evaluations. A de novo Markov model was developed to determine the cost-effectiveness of TCD ultrasonography and blood transfusion, where clinically appropriate, in patients with SCD. Two randomised controlled trials met the inclusion criteria involving a study population of 209 participants. One compared blood transfusion with standard care for children who are identified as being at high risk of stroke using TCD ultrasonography. In this trial, one patient in the transfusion group had a stroke (1/63) compared with 11 children in the standard care group (11/67). The other trial assessed the impact of halting chronic transfusion in patients with SCD. Sixteen patients in the transfusion-halted group had an event (16/41) (two patients experienced stroke and 14 reverted to abnormal TCD velocity); there were no events in the continued-transfusion group (0/38). No meta-analyses of these trials were undertaken. No relevant economic evaluations were identified for inclusion in the review. The de novo modelling suggests that blood transfusions plus TCD scans (compared with just TCD scans) for patients with SCD at high risk of stroke, aged ≥ 2 years, may be good value for money. The intervention has an incremental cost-effectiveness ratio of £24,075 per quality-adjusted life-year gained, and helps avoid 68 strokes over the lifetime of a population of 1000 patients. The intervention costs an additional £13,751 per patient and generates 0.6 extra years of life in full health per patient. The data available for the economic analysis are limited. Sensitivity analyses and validation against existing data and expert opinion provide some reassurance that the conclusion of the model is reliable but further research is required to validate these findings. The main limitations relate to the availability of published clinical data; no completed randomised controlled trials were identified which evaluated the efficacy of either BMT or hydroxycarbamide for primary stroke prevention. Both the clinical and cost data available for use in the economic analysis are limited. Sensitivity analyses and validation against existing data and expert opinion provide some reassurance that the conclusions of the model are reliable, but further research is required to validate these findings. The use of TCD ultrasonography to identify children at high risk of stroke, and treating these children with prophylactic blood transfusions, appears to be both clinically effective and cost-effective compared with TCD ultrasonography only. However, given the limitations in the data available, further research is required to verify this conclusion. Several research recommendations can be proposed from this review. Clinically, more research is needed to assess the effects and optimal duration of long-term blood transfusion and the potential role of hydroxycarbamide in primary stroke prevention. From an economics perspective, further research is required to generate more robust data on which to base estimates of cost-effectiveness or against which model outputs can be calibrated. More data are required to explain how utility weights vary with age, transfusions and strokes. Research is also needed around the cost of paediatric stroke in the UK. PROSPERO CRD42011001496. The National Institute for Health Research Health Technology Assessment programme.

Elevated local skin temperature impairs cutaneous vasoconstrictor responses to a simulated haemorrhagic challenge while heat stressed

During a simulated haemorrhagic challenge, syncopal symptoms develop sooner when individuals are hyperthermic relative to normothermic. This is due, in part, to a large displacement of blood to the cutaneous circulation during hyperthermia, coupled with inadequate cutaneous vasoconstriction during the hypotensive challenge. The influence of local skin temperature on these cutaneous vasoconstrictor responses is unclear. This project tested the hypothesis that local skin temperature modulates cutaneous vasoconstriction during simulated haemorrhage in hyperthermic humans. Eight healthy participants (four men and four women; 32 ± 7 years old; 75.2 ± 10.8 kg) underwent lower-body negative pressure to presyncope while heat stressed via a water-perfused suit sufficiently to increase core temperature by 1.2 ± 0.2 °C. At forearm skin sites distal to the water-perfused suit, local skin temperature was either 35.2 ± 0.6 (mild heating) or 38.2 ± 0.2 °C (moderate heating) throughout heat stress and lower-body negative pressure, and remained at these temperatures until presyncope. The reduction in cutaneous vascular conductance during the final 90 s of lower-body negative pressure, relative to heat-stress baseline, was greatest at the mildly heated site (-10 ± 15% reduction) relative to the moderately heated site (-2 ± 12%; P = 0.05 for the magnitude of the reduction in cutaneous vascular conductance between sites), because vasoconstriction at the moderately heated site was either absent or negligible. In hyperthermic individuals, the extent of cutaneous vasoconstriction during a simulated haemorrhage can be modulated by local skin temperature. In situations where skin temperature is at least 38 °C, as is the case in soldiers operating in warm climatic conditions, a haemorrhagic insult is unlikely to be accompanied by cutaneous vasoconstriction.

Influence of sympathoexcitation at high altitude on cerebrovascular function and ventilatory control in humans

We sought to determine the influence of sympathoexcitation on dynamic cerebral autoregulation (CA), cerebrovascular reactivity, and ventilatory control in humans at high altitude (HA). At sea level (SL) and following 3-10 days at HA (5,050 m), we measured arterial blood gases, ventilation, arterial pressure, and middle cerebral blood velocity (MCAv) before and after combined α- and β-adrenergic blockade. Dynamic CA was quantified using transfer function analysis. Cerebrovascular reactivity was assessed using hypocapnia and hyperoxic hypercapnia. Ventilatory control was assessed from the hypercapnia and during isocapnic hypoxia. Arterial Pco(2) and ventilation and its control were unaltered following blockade at both SL and HA. At HA, mean arterial pressure (MAP) was elevated (P < 0.01 vs. SL), but MCAv remained unchanged. Blockade reduced MAP more at HA than at SL (26 vs. 15%, P = 0.048). At HA, gain and coherence in the very-low-frequency (VLF) range (0.02-0.07 Hz) increased, and phase lead was reduced (all P < 0.05 vs. SL). Following blockade at SL, coherence was unchanged, whereas VLF phase lead was reduced (-40 ± 23%; P < 0.01). In contrast, blockade at HA reduced low-frequency coherence (-26 ± 20%; P = 0.01 vs. baseline) and elevated VLF phase lead (by 177 ± 238%; P < 0.01 vs. baseline), fully restoring these parameters back to SL values. Irrespective of this elevation in VLF gain at HA (P < 0.01), blockade increased it comparably at SL and HA (∼43-68%; P < 0.01). Despite elevations in MCAv reactivity to hypercapnia at HA, blockade reduced (P < 0.05) it comparably at SL and HA, effects we attributed to the hypotension and/or abolition of the hypercapnic-induced increase in MAP. With the exception of dynamic CA, we provide evidence of a redundant role of sympathetic nerve activity as a direct mechanism underlying changes in cerebrovascular reactivity and ventilatory control following partial acclimatization to HA. These findings have implications for our understanding of CBF function in the context of pathologies associated with sympathoexcitation and hypoxemia.

Continual Transcranial Doppler in the Monitoring of Hemodynamic Change following Aneurysmal Subarachnoid Hemorrhage

To analyze and compare the value of different treatment methods for acute aneurysmal subarachnoid hemorrhage (aSAH)-related vasospasm. Cerebral hemodynamic variables' changes were evaluated by transcranial Doppler (TCD) in aSAH patients within 14 days after onset. Thirty aSAH patients were enrolled in the study within 72 h after onset. Baseline CT and TCD were used for assessment. Patients were divided into three groups according to SAH severity and patients' discretion: nonsurgical group, endovascular coiling, and neurosurgical clipping. TCD hemodynamic parameters were measured and Lindegaard index was calculated daily from onset to 14th day after SAH. The group mean cerebral blood velocity (MBFV) and Lindegaard index were compared using repeated measures analysis of variance (reANOVA). Least Significant Difference (LSD) test was used for post hoc comparison. All 30 patients were followed for 90 days after onset for outcome assessment. The values of MBFV and Lindegaard index of anterior cerebral artery (ACA)/middle cerebral artery (MCA) from high to low is nonsurgical group, clipping and coiling (ACA: P= 0.0001/P= 0.006; MCA: P= 0.243/P= 0.317). These results indicate that both neurosurgical clipping and endovascular coiling management may relieve the severity of cerebral vasospasm in acute aSAH.

Effect of Head Rotation on Cerebral Blood Velocity in the Prone Position

Background. The prone position is applied to facilitate surgery of the back and to improve oxygenation in the respirator-treated patient. In particular, with positive pressure ventilation the prone position reduces venous return to the heart and in turn cardiac output (CO) with consequences for cerebral blood flow. We tested in healthy subjects the hypothesis that rotating the head in the prone position reduces cerebral blood flow. Methods. Mean arterial blood pressure (MAP), stroke volume (SV), and CO were determined, together with the middle cerebral artery mean blood velocity (MCA Vmean) and jugular vein diameters bilaterally in 22 healthy subjects in the prone position with the head centered, respectively, rotated sideways, with and without positive pressure breathing (10 cmH2O). Results. The prone position reduced SV (by 5.4 ± 1.5%; P < 0.05) and CO (by 2.3 ± 1.9 %), and slightly increased MAP (from 78 ± 3 to 80 ± 2 mmHg) as well as bilateral jugular vein diameters, leaving MCA Vmean unchanged. Positive pressure breathing in the prone position increased MAP (by 3.6 ± 0.8 mmHg) but further reduced SV and CO (by 9.3 ± 1.3 % and 7.2 ± 2.4 % below baseline) while MCA Vmean was maintained. The head-rotated prone position with positive pressure breathing augmented MAP further (87 ± 2 mmHg) but not CO, narrowed both jugular vein diameters, and reduced MCA Vmean (by 8.6 ± 3.2 %). Conclusion. During positive pressure breathing the prone position with sideways rotated head reduces MCA Vmean ~10% in spite of an elevated MAP. Prone positioning with rotated head affects both CBF and cerebrovenous drainage indicating that optimal brain perfusion requires head centering.

Kinetics of exercise‐induced neural activation; interpretive dilemma of altered cerebral perfusion

Neural activation decreases cerebral deoxyhaemoglobin (HHb(C)) and increases oxyhaemoglobin concentration (O(2)Hb(C)). In contrast, patients who present with restricted cerebral blood flow, such as those suffering from cerebral ischaemia or Alzheimer's disease, and during the course of ageing the converse occurs, in that HHb(C) increases and O(2)Hb(C) decreases during neural activation. In the present study, we examined the interpretive implications of altered exercise-induced cerebral blood flow for cortical oxygenation in healthy subjects. Both O(2)Hb(C) and HHb(C) (prefrontal cortex) were determined in 11 healthy men using near-infrared spectroscopy (NIRS). Middle cerebral artery mean blood velocity (MCA V(mean)) was determined via transcranial Doppler ultrasonography. Measurements were performed during contralateral hand-grip exercise during suprasystolic bilateral thigh-cuff occlusion (Cuff+) and within 2 s of cuff release (Cuff-) for the acute manipulation of cerebral perfusion. During Cuff+, both MCA V(mean) and O(2)Hb(C) increased during exercise, whereas HHb(C) decreased. In contrast, the opposite occurred during the Cuff- manipulation. These findings highlight the inverse relationship between cerebral blood flow and cerebral oxygenation as determined by NIRS, which has interpretive implications for the kinetics underlying exercise-induced neural activation.