Middle Cerebral Artery Velocity Research Articles

Prediction of Cerebral Hyperperfusion Syndrome with Velocity Blood Pressure Index.

Background:Cerebral hyperperfusion syndrome is an important complication of carotid endarterectomy (CEA). An >100% increase in middle cerebral artery velocity (MCAV) after CEA is used to predict the cerebral hyperperfusion syndrome (CHS) development, but the accuracy is limited. The increase in blood pressure (BP) after surgery is a risk factor of CHS, but no study uses it to predict CHS. This study was to create a more precise parameter for prediction of CHS by combined the increase of MCAV and BP after CEA.Methods:Systolic MCAV measured by transcranial Doppler and systematic BP were recorded preoperatively; 30 min postoperatively. The new parameter velocity BP index (VBI) was calculated from the postoperative increase ratios of MCAV and BP. The prediction powers of VBI and the increase ratio of MCAV (velocity ratio [VR]) were compared for predicting CHS occurrence.Results:Totally, 6/185 cases suffered CHS. The best-fit cut-off point of 2.0 for VBI was identified, which had 83.3% sensitivity, 98.3% specificity, 62.5% positive predictive value and 99.4% negative predictive value for CHS development. This result is significantly better than VR (33.3%, 97.2%, 28.6% and 97.8%). The area under the curve (AUC) of receiver operating characteristic: AUCVBI= 0.981, 95% confidence interval [CI] 0.949–0.995; AUCVR= 0.935, 95% CI 0.890–0.966, P = 0.02.Conclusions:The new parameter VBI can more accurately predict patients at risk of CHS after CEA. This observation needs to be validated by larger studies.

Restoring heat stress-associated reduction in middle cerebral artery velocity does not reduce fatigue in the heat.

Heat-induced hyperventilation may reduce PaCO2 and thereby cerebral perfusion and oxygenation and in turn exercise performance. To test this hypothesis, eight volunteers completed three incremental exercise tests to exhaustion: (a) 18 °C ambient temperature (CON); (b) 38 °C (HEAT); and (c) 38 °C with addition of CO2 to inspiration to prevent the hyperventilation-induced reduction in PaCO2 (HEAT + CO2 ). In HEAT and HEAT + CO2 , rectal temperature was elevated prior to the exercise tests by means of hot water submersion and was higher (P < 0.05) than in CON. Compared with CON, ventilation was elevated (P < 0.01), and hence, PaCO2 reduced in HEAT. This caused a reduction (P < 0.05) in mean cerebral artery velocity (MCAvmean ) from 68.6 ± 15.5 to 53.9 ± 10.0 cm/s, which was completely restored in HEAT + CO2 (68.8 ± 5.8 cm/s). Cerebral oxygenation followed a similar pattern. V ˙ O 2 m a x was 4.6 ± 0.1 L/min in CON and decreased (P < 0.05) to 4.1 ± 0.2 L/min in HEAT and remained reduced in HEAT + CO2 (4.1 ± 0.2 L/min). Despite normalization of MCAvmean and cerebral oxygenation in HEAT + CO2 , this did not improve exercise performance, and thus, the reduced MCAvmean in HEAT does not seem to limit exercise performance.

Impact of transient hypotension on regional cerebral blood flow in humans.

We examined the impact of progressive hypotension with and without hypocapnia on regional extracranial cerebral blood flow (CBF) and intracranial velocities. Participants underwent progressive lower-body negative pressure (LBNP) until pre-syncope to inflict hypotension. End-tidal carbon dioxide was clamped at baseline levels (isocapnic trial) or uncontrolled (poikilocapnic trial). Middle cerebral artery (MCA) and posterior cerebral artery (PCA) blood velocities (transcranial Doppler; TCD), heart rate, blood pressure and end-tidal carbon dioxide were obtained continuously. Measurements of internal carotid artery (ICA) and vertebral artery (VA) blood flow (ICABF and VABF respectively) were also obtained. Overall, blood pressure was reduced by ~20% from baseline in both trials (P<0.001). In the isocapnic trial, end-tidal carbon dioxide was successfully clamped at baseline with hypotension, whereas in the poikilocapnic trial it was reduced by 11.1 mmHg (P<0.001) with hypotension. The decline in the ICABF with hypotension was comparable between trials (-139 ± 82 ml; ~30%; P<0.0001); however, the decline in the VABF was -28 ± 22 ml/min (~21%) greater in the poikilocapnic trial compared with the isocapnic trial (P=0.002). Regardless of trial, the blood flow reductions in ICA (-26 ± 14%) and VA (-27 ± 14%) were greater than the decline in MCA (-21 ± 15%) and PCA (-19 ± 10%) velocities respectively (P ≤ 0.01). Significant reductions in the diameter of both the ICA (~5%) and the VA (~7%) contributed to the decline in cerebral perfusion with systemic hypotension, independent of hypocapnia. In summary, our findings indicate that blood flow in the VA, unlike the ICA, is sensitive to changes hypotension and hypocapnia. We show for the first time that the decline in global CBF with hypotension is influenced by arterial constriction in the ICA and VA. Additionally, our findings suggest TCD measures of blood flow velocity may modestly underestimate changes in CBF during hypotension with and without hypocapnia, particularly in the posterior circulation.

Effect of Prior Use Menopausal Hormone Therapy on Blood Pressure Responses in Women

Cerebrovascular reactivity to hypercapnia is higher in women receiving menopausal hormone therapy (MHT) compared with controls, and this may persist after cessation of MHT. We hypothesized that the effect of MHT may be influenced by mean arterial pressure (MAP). Therefore, we examined both middle cerebral artery velocity (MCAv) and MAP responses to stepped hypercapnia in 60 postmenopausal women who were previously randomized to receive oral conjugated equine estrogen (oCEE, n=15), transdermal 17β estradiol (tE2, n=22), or placebo (PLA, n=23) for 4 years. After a 3 year washout period, reactivity was calculated from the slope of the relationship between MCAv or MAP and end‐tidal CO2. MCAv reactivity was higher in the oCEE group compared with the PLA group (1.6±0.2 vs. 1.1±0.1 cm/s/mmHg; oCEE vs. PLA, respectively, p&lt;0.05), but similar between the tE2 and PLA group (1.3±0.2 vs. 1.1±0.1 cm/s/mmHg; tE2 vs. PLA, respectively, p&gt;0.05). There were no significant differences in MAP reactivity (1.0±0.2, 0.6±0.1, 0.7±0.2 mmHg/mmHg of CO2, oCEE vs. tE2 vs. PLA, respectively, p&gt;0.05) among the groups. However, in the combined MHT group, MAP reactivity was positively correlated with MCAv reactivity (r=0.58, p&lt;0.001), such that women with higher MAP responses demonstrate greater MCAv responses to hypercapnia. In conclusion, there were no differences in MAP reactivity 3 years after cessation of MHT. In addition, our results suggest that greater cerebrovascular reactivity in postmenopausal women who received MHT may be driven by augmented blood pressure responses to hypercapnia. Funding: K99 HL 118164, AG 044170 and HL 83947.

Cerebral Blood Flow Regulation Following Inhalation of Nicotine via Electronic Cigarettes

Background The use of electronic cigarettes (e-cigarettes) is growing rapidly but the physiologic effects of vaporized nicotine are relatively unknown. We hypothesized that acute inhalation of vaporized nicotine via e-cigarettes would impair regulation of cerebral blood flow (CBF) in response to variations in arterial pressure (cerebral autoregulation, CA). Methods: 13 subjects (6 F; 7 M) inhaled vapor from an 18 mg nicotine (nicotine) or a 0 mg nicotine (placebo) e-cigarette on separate days (randomized). Heart rate (HR), mean arterial pressure (MAP), mean middle cerebral artery velocity (MCAv), and cerebral oxygen saturation (SCO2) were measured non-invasively. Oscillatory lower body negative pressure (OLBNP) between 0 and -60 mmHg was applied for 20 cycles at 0.05 Hz and 0.10 Hz. Results: Between placebo and nicotine conditions, baseline MAP, MCAv, SCO2, and HR were similar (P蠅0.21). MAP and ScO2 very low frequency (VLF; 0.04-0.07 Hz) power with 0.05 Hz OLBNP, and low frequency (LF; 0.07-0.2 Hz) power with 0.1 Hz OLBNP were higher under the placebo condition (P蠄0.03-0.06). Cross-spectral analysis in the LF (with 0.1 Hz OLBNP) and VLF (with 0.05 Hz OLBNP) revealed that gain between MAP-MCAv was similar between conditions (P蠅0.128). MCAv-ScO2 and MAP-ScO2 coherences were <0.5 under all conditions, so gain values are not reported. Conclusion These data suggest that nicotine, when acutely inhaled via e-cigarettes, does not impair the cerebral pressure-flow relationship. Funding: University of Texas at San Antonio (UTSA) Collaborative Seed Grant.

Hypoxic Cerebral Vasodilation in Healthy and Metabolic Syndrome Adults: Distinct Interactions between Cyclooxygenase and Reactive Oxygen Species Signaling

Excess reactive oxygen species (ROS) limit hypoxia‐mediated cerebral vasodilation in animal models of metabolic syndrome (MetSyn). Cyclooxygenase (COX) may be a source of ROS, but data are lacking in humans. We hypothesized ROS limit hypoxic cerebral vasodilation in human MetSyn, but COX is not the source. We measured middle cerebral artery velocity (MCAv) with transcranial Doppler ultrasound in 12 MetSyn adults (34±2 yr) and 12 healthy adults (28±1 yr) during baseline and steady‐state hypoxia (SPo2=80%). Intravenous ascorbic acid suppressed ROS during the first steady‐state hypoxia. Oral indomethacin was administered to inhibit COX prior to a second hypoxia trial to investigate the combined roles of ROS and COX during hypoxia. MCAv was normalized for MABP as cerebrovascular conductance index [CVCi = (MCAv ÷ MABP) * 100], and a change in CVCi from baseline (ΔCVCi) indicated hypoxic dilation. ΔCVCi was ~50% lower in adults with MetSyn during control hypoxia (p&lt;0.05). Ascorbic acid infusion increased ΔCVCi in MetSyn adults (p&lt;0.05), but not healthy adults. Combined ascorbic acid and indomethacin increased ΔCVCi in MetSyn adults (p&lt;0.05) similar to ascorbic acid alone. Surprisingly in healthy adults, combined ascorbic acid and indomethacin reduced ΔCVCi by ~75% (p&lt;0.05). This contrasts previous data in healthy adults that indicated no effect of indomethacin alone. In summary, healthy adults express a ROS‐COX redundancy, whereby ROS suppression increased reliance on COX products to achieve hypoxic cerebral vasodilation. MetSyn disrupts this complementary role of ROS, such that COX‐derived ROS restrain hypoxic cerebral vasodilation.

Coupling between arterial pressure, cerebral blood velocity, and cerebral tissue oxygenation with spontaneous and forced oscillations

We tested the hypothesis that transmission of arterial pressure to brain tissue oxygenation is low under conditions of arterial pressure instability. Two experimental models of hemodynamic instability were used in healthy human volunteers; (1) oscillatory lower body negative pressure (OLBNP) (N = 8; 5 male, 3 female), and; (2) maximal LBNP to presyncope (N = 21; 13 male, 8 female). Mean arterial pressure (MAP), middle cerebral artery velocity (MCAv), and cerebral tissue oxygen saturation (ScO2) were measured non-invasively. For the OLBNP protocol, between 0 and −60 mmHg negative pressure was applied for 20 cycles at 0.05 Hz, then 20 cycles at 0.1 Hz. For the maximal LBNP protocol, progressive 5 min stages of chamber decompression were applied until the onset of presyncope. Spectral power of MAP, mean MCAv, and ScO2 were calculated within the VLF (0.04–0.07 Hz), and LF (0.07–0.2 Hz) ranges, and cross-spectral coherence was calculated for MAP-mean MCAv, MAP-ScO2, and mean MCAv-ScO2 at baseline, during each OLBNP protocol, and at the level prior to pre-syncope during maximal LBNP (sub-max). The key findings are (1) both 0.1 Hz OLBNP and sub-max LBNP elicited increases in LF power for MAP, mean MCAv, and ScO2 (p ≤ 0.08); (2) 0.05 Hz OLBNP increased VLF power in MAP and ScO2 only (p ≤ 0.06); (3) coherence between MAP-mean MCAv was consistently higher (≥0.71) compared with MAP-ScO2, and mean MCAv-ScO2 (≤0.43) during both OLBNP protocols, and sub-max LBNP (p ≤ 0.04). These data indicate high linearity between pressure and cerebral blood flow variations, but reduced linearity between cerebral tissue oxygenation and both arterial pressure and cerebral blood flow. Measuring arterial pressure variability may not always provide adequate information about the downstream effects on cerebral tissue oxygenation, the key end-point of interest for neuronal viability.

Effect of occlusal reconstruction on cerebral blood flow and cerebral oxygen saturation in patients with malocclusion

To investigate the effect of occlusal reconstruction on blood flow velocity and cerebral oxygen saturation in patients with malocclusion. Thirty-three patients with malocclusion treated with occlusal reconstruction in Department of Stomatology, Medical School of Huzhou Normal College from Feb 2011 to Oct 2013 were enrolled in the study. The systolic peak flow velocity (vs), end-diastolic peak flow (vd) , mean peak flow velocity (vm) of middle cerebral artery and the oxygen saturation (rScO2) in the brain were detected at rest or chewing status by using transcranial Doppler color ultrasonography and near-infrared spectroscopy, respectively. In rest state, vm was significantly increased on 3 months after treatment, while vs and vd were significantly increased on 6 months after treatment and rScO2 were increased on 12 months after treatment (P<0.05). In chewing state, vs, vm, and rScO2 were increased on 3 months after treatment, and vd was increased on 6 months after treatment (P<0.05). Occlusal reconstruction can increase blood flow velocity of middle cerebral artery and cerebral oxygen saturation and improve oxygen supply of the brain in patients with malocclusion.

Comparative efficacy of meloxicam and placebo in vasospasm of patients with subarachnoid hemorrhage.

Cerebral vasospasm considered to be a serious cause of morbidity and mortality following subarachnoid haemorrhage (SAH).Despite several available therapeutic options, current protocols do not prevent major consequences of vasospasm. Inflammation is believed to play an important role in post-haemorrhagic vasospasm. Meloxicam is a non-steroidal anti-inflammatory drug. The aim of this study was to compare the efficacy of meloxicam versus placebo on vasospasm in patients with SAH. In this randomized, double-blind, placebo-controlled trial, SAH patients randomly received 7.5 mg meloxicam or placebo twice daily for 7 days. End points were, middle cerebral artery velocity obtained with transcranial doppler, in-hospital mortality, hospital stay and discharge Glasgow Outcome Scale. Eighty-one patients enrolled in the study. (40 received meloxicam, 41 received placebo). Baseline characteristics were similar between the groups. There were no differences in length of hospitalization (17.4 ± 3.1 vs 18.6 ± 4.2 days; p = 0.145), in-hospital mortality rate (15 vs 22%; p-value=0.569), or GOS (p = 0.972) between the two groups. MCA velocity were slightly less in patients who had received meloxicam, but not to a significant degree (p-value=0. 564(. No side effect has been detected for meloxicam. This study did not prove meloxicam efficacy in vasospasm of SAH patients. But it demonstrated that clinical trial of meloxicam in these patients is feasible and probably safe. The effectiveness of meloxicam on cerebral vasospasm has to be studied in larger trials.

Effects of noise and mental task performance upon changes in cerebral blood flow parameters.

The objectives of this paper were to determine whether traffic noise influences the parameters of cerebral blood flow (CBF) measured by functional transcranial Doppler sonography (fTCD) during the performance of mental tasks, and to see whether impact of noise on CBF changes with age. The study comprised 36 healthy volunteers, 22 women and 14 men, aged 25-49 years. The fTCD was performed using a fixed 2-MHz probe, aiming for an evaluation of mean velocity (MFV) and the pulsatility index (PI) in the middle cerebral artery (MCA) on both sides. Subsequently, fTCD was monitored: At rest; during performance of the Paced Auditory Serial Addition Test (PASAT); during exposure to traffic noise; and during concomitant exposure to noise and PASAT performance. MFV and PI were compared for particular conditions and correlated with age. During exposure to noise, flow parameters did not change significantly. PASAT performance in silence increased MFV and decreased PI in MCA on both sides. During PASAT performance, on exposure to noise, MCV and PI changed significantly only in the left MCA. However, values of MFV were significantly lower during noise than in silence. Correlations with age were noted for velocities in the right MCA during PASAT performance in silence and for PI on both sides during PASAT performed in noise conditions. Noise impairs the CBF during mental tasks. A comparison of changes in CBF parameters correlated with age suggests that the involvement of the nondominant hemisphere in managing with noise effects increases with age.

Two-week normobaric intermittent-hypoxic exposures stabilize cerebral perfusion during hypocapnia and hypercapnia.

The effect of moderately extended, intermittent-hypoxia (IH) on cerebral perfusion during changes in CO2 was unknown. Thus, we assessed the changes in cerebral vascular conductance (CVC) and cerebral tissue oxygenation (ScO2) during experimental hypocapnia and hypercapnia following 14-day normobaric exposures to IH (10% O2). CVC was estimated from the ratio of mean middle cerebral arterial blood flow velocity (transcranial Doppler sonography) to mean arterial pressure (tonometry), and ScO2 in the prefrontal cortex was monitored by near-infrared spectroscopy. Changes in CVC and ScO2 during changes in partial pressure of end-tidal CO2 (PETCO2, mass spectrometry) induced by 30-s paced-hyperventilation (hypocapnia) and during 6-min CO2 rebreathing (hypercapnia) were compared before and after 14-day IH exposures in eight young nonsmokers. Repetitive IH exposures reduced the ratio of %ΔCVC/ΔPETCO2 during hypocapnia (1.00 ± 0.13 vs 1.94 ± 0.35 vs %/mmHg, P = 0.026) and the slope of ΔCVC/ΔPETCO2 during hypercapnia (1.79 ± 0.37 vs 2.97 ± 0.64 %/mmHg, P = 0.021), but had no significant effect on ΔScO2/ΔPETCO2. The ventilatory response to hypercapnia during CO2 rebreathing was significantly diminished following 14-day IH exposures (0.83 ± 0.07 vs 1.14 ± 0.09 L/min/mmHg, P = 0.009). We conclude that repetitive normobaric IH exposures significantly diminish variations of cerebral perfusion in response to hypercapnia and hypocapnia without compromising cerebral tissue oxygenation. This IH-induced blunting of cerebral vasoreactivity during CO2 variations helps buffer excessive oscillations of cerebral underperfusion and overperfusion while sustaining cerebral O2 homeostasis.

Cerebral oxygenation in health and disease.

Monitoring cerebral blood flow (CBF) and oxygenation has implications for both clinical practice and research interests; e.g., to provide insight into functional neurovascular coupling, to better understand orthostatic hypotension, and to evaluate the influence of vasopressors on cerebral oxygenation during anesthesia and/or surgery. These topics, and others, are addressed in this e-book by presenting original research, reviews, and opinion papers covering new, exciting but also controversial issues related to cerebral oxygenation in health and disease as evaluated by near-infrared spectroscopy (NIRS).

Cardiovascular and cerebrovascular responses to progressive central hypovolemia in young smokers: a preliminary study.

The purpose of this study was to describe cardiovascular and cerebrovascular responses of smokers and nonsmokers to progressive central hypovolemia. Twenty subjects participated (equal male and female). We recorded the electrocardiogram, beat-to-beat arterial pressure (Finometer), cerebral blood velocity of the middle cerebral artery (transcranial Doppler), and end-tidal CO2. Lower body negative pressure (LBNP) was applied at 3 mm Hg · min(-1) for 20 minutes to an ending pressure of -60 mm Hg, and data were averaged in 2-minute bins. Arterial pressures were similar between groups at baseline, but heart rates tended to be higher, and stroke volumes and cerebral velocities tended to be lower in smokers at baseline and during LBNP (all p ≥ 0.17). Heart rates increased, and arterial pressures, stroke volumes, and cerebral velocities decreased during LBNP (all p ≤ 0.05), but responses were not different between smokers and nonsmokers. During the final stage of LBNP, systolic pressures and mean middle cerebral artery velocities were substantially lower in smokers than nonsmokers: these preliminary data may suggest clinical relevance of smoking status, but the magnitude of differences between groups were not distinguishable statistically. We therefore conclude that smokers and nonsmokers respond similarly to progressive central hypovolemia.

Study of neurovascular coupling during cold pressor test in patients with migraine.

Altered neurovascular coupling in migraineurs could be a consequence of impaired function of modulatory brainstem nuclei. The cold pressor test (CPT) should activate brainstem structures. We measured visually evoked cerebral blood flow velocity response (VEFR) to CPT in migraine. Twenty-three healthy volunteers and 29 migraineurs participated in the study. We measured arterial blood pressure, end-tidal CO2, heart rate and cerebral blood flow velocity in posterior and middle cerebral artery using transcranial Doppler. VEFR was calculated as cerebrovascular reactivity to photic stimulation before, during and after CPT. In healthy individuals, there was a significant decrease in peak systolic VEFR from CPT phase to recovery phase (p < 0.05). There was an increase in mean VEFR from basal to CPT phase and a decrease from CPT to recovery phase, both significant (p < 0.05). End-diastolic VEFR increased from basal to CPT phase and decreased in recovery phase below the basal phase values, all changes significant (p < 0.05). In migraine, no statistically significant changes in peak systolic, mean or end-diastolic VEFRs were observed between phases (p > 0.05). The differences in phases in mean and end-diastolic VEFRs between the basal phase and the CPT phase and between the CPT phase and the recovery phase were significantly higher in healthy individuals (p < 0.05). The absence of the effect of CPT on VEFR in migraine is likely to be a consequence of impaired subcortical modulation of neurovascular coupling.

Relationship between cerebral blood flow and blood pressure in long-term heart transplant recipients.

Heart transplant recipients are at an increased risk for cerebral hemorrhage and ischemic stroke; yet, the exact mechanism for this derangement remains unclear. We hypothesized that alterations in cerebrovascular regulation is principally involved. To test this hypothesis, we studied cerebral pressure-flow dynamics in 8 clinically stable male heart transplant recipients (62±8 years of age and 9±7 years post transplant, mean±SD), 9 male age-matched controls (63±8 years), and 10 male donor controls (27±5 years). To increase blood pressure variability and improve assessment of the pressure-flow dynamics, subjects performed squat-stand maneuvers at 0.05 and 0.10 Hz. Beat-to-beat blood pressure, middle cerebral artery velocity, and end-tidal carbon dioxide were continuously measured during 5 minutes of seated rest and throughout the squat-stand maneuvers. Cardiac baroreceptor sensitivity gain and cerebral pressure-flow responses were assessed with linear transfer function analysis. Heart transplant recipients had reductions in R-R interval power and baroreceptor sensitivity low frequency gain (P<0.01) compared with both control groups; however, these changes were unrelated to transfer function metrics. Thus, in contrast to our hypothesis, the increased risk of cerebrovascular complication after heart transplantation does not seem to be related to alterations in cerebral pressure-flow dynamics. Future research is, therefore, warranted.

Influence of nocturnal and daytime sleep on initial orthostatic hypotension.

The incidence of vasovagal syncope is more common in the morning. Previous researchers have reported negligible diurnal variation in the physiological responses associated with initial orthostatic hypotension (IOH). Nevertheless, physical activity and sleep prior to morning and afternoon test times have not been controlled and may influence the findings. We designed a semi-constant routine protocol to examine diurnal variation in cardiorespiratory and cerebrovascular responses to active standing. At 06:00 and 16:00 hours, nine males (27 ± 9 years) completed an upright-stand protocol. Altimetry-measured sleep durations were 3.3 ± 0.4 and 3.2 ± 0.6 h immediately prior to the morning and afternoon test times. Continuous beat-to-beat measurements of middle cerebral artery velocity (MCAv), mean arterial blood pressure (MAP), heart rate (HR), and end-tidal carbon dioxide were obtained. Intestinal body temperature and salivary melatonin concentrations were also measured. Compared with the afternoon, resting HR and body temperature were 4 ± 2 beats min(-1) and 0.45 ± 0.2 °C lower, respectively, whereas melatonin concentration was 28.7 ± 3.2 pg ml(-1) higher in the morning (P ≤ 0.02). Although all individuals experienced IOH at both times of the day, the initial decline in MAP during standing was 13 ± 4 mmHg greater in the afternoon (P = 0.01). Nevertheless, the decline in MCAv was comparable at both times of day (mean difference: 2 ± 3 cm s(-1); P = 0.5). These findings indicate that a bout of sleep in the afternoon in healthy young individuals results in greater IOH that is compensated for by effective cerebral blood flow regulation.

The effects of transcranial LED therapy (TCLT) on cerebral blood flow in the elderly women.

During aging processes, there is a range of functional changes, where we can highlight the disease related to the central nervous system, such as Alzheimer disease and others forms of dementia. This study investigated the effects of transcranial light emitting diode (LED) on cerebral blood flow in healthy elderly women analyzed by transcranial Doppler ultrasound (TCD) of the right and left middle cerebral artery and basilar artery. Twenty-five noninstitutionalized elderly women (mean age 72 years old), with a cognitive status >24, were assessed using transcranial Doppler ultrasound on two separate occasions: pre-irradiation and post-transcranial LED therapy (TCLT). Prior to this, they answered two questionnaires: the perceived stress scale and the general health questionnaire. TCLT (627 nm, 70 mW/cm(2), 10 J/cm(2)) was performed at four points of the frontal and parietal region for 30 s each, totaling 120 s two times per week for 4 weeks. Paired t-test results showed that there was a significant improvement after TCLT with increase in the systolic and diastolic velocity of the left middle cerebral artery (25 and 30%, respectively) and basilar artery (up to 17 and 25%), as well as a decrease in the pulsatility index and resistance index values of the three cerebral arteries analyzed (p < 0.05). TCD parameters showed improvement in the blood flow on the arteries analyzed. TCLT promoted a blood and vasomotor behavior of the basilar and middle cerebral arteries in healthy elderly women.

On the limits of cerebral oxygen extraction.

On the limits of cerebral oxygen extraction.

Cerebrovascular responses during rowing: Do circadian rhythms explain morning and afternoon performance differences?

The purpose of this study was to characterize cerebrovascular responses to rowing exercise, investigating whether their diurnal variation might explain performance differences across a day. Twelve male rowers completed incremental rowing exercise and a 2000-m ergometer time trial at 07:00 h and 16:00 h, 1 week apart, while middle cerebral artery velocity (MCAv), cerebral (prefrontal), and muscular (vastus lateralis) tissue oxygenation and hemoglobin volume (via near-infrared spectroscopy), heart rate, and pressure of end-tidal CO2 (PET CO2) were recorded. MCAv was 20-25% above resting levels (68 ± 12 cm/s) during submaximal and maximal exercise intensities, despite PET CO2 being reduced during maximal efforts (down ∼ 0.5-0.8 kPa); thus revealing a different perfusion profile to the inverted-U observed in other exercise modes. The afternoon time trial was 3.4 s faster (95% confidence interval 0.9-5.8 s) and mean power output 3.2% higher (337 vs 347 W; P = 0.04), in conjunction with similar exercise-induced elevations in MCAv (P = 0.60) and reductions in cerebral oxygenation (TOI) (P = 0.12). At the muscle, afternoon trials involved similar oxygen extraction (HHb volume and TOI) albeit from a relatively lower total Hb volume (P < 0.01). In conclusion, rowing performance was better in the afternoon, but not in conjunction with differences in MCAv or exercise-induced differences in cerebral oxygenation.

Electromyographic, cerebral, and muscle hemodynamic responses during intermittent, isometric contractions of the biceps brachii at three submaximal intensities.

This study examined the electromyographic, cerebral and muscle hemodynamic responses during intermittent isometric contractions of biceps brachii at 20, 40, and 60% of maximal voluntary contraction (MVC). Eleven volunteers completed 2 min of intermittent isometric contractions (12/min) at an elbow angle of 90° interspersed with 3 min rest between intensities in systematic order. Surface electromyography (EMG) was recorded from the right biceps brachii and near infrared spectroscopy (NIRS) was used to simultaneously measure left prefrontal and right biceps brachii oxyhemoglobin (HbO2), deoxyhemoglobin (HHb), and total hemoglobin (Hbtot). Transcranial Doppler ultrasound was used to measure middle cerebral artery velocity (MCAv) bilaterally. Finger photoplethysmography was used to record beat-to-beat blood pressure and heart rate. EMG increased with force output from 20 to 60% MVC (P < 0.05). Cerebral HbO2 and Hbtot increased while HHb decreased during contractions with differences observed between 60% vs. 40% and 20% MVC (P < 0.05). Muscle HbO2 decreased while HHb increased during contractions with differences being observed among intensities (P < 0.05). Muscle Hbtot increased from rest at 20% MVC (P < 0.05), while no further change was observed at 40 and 60% MVC (P > 0.05). MCAv increased from rest to exercise but was not different among intensities (P > 0.05). Force output correlated with the root mean square EMG and changes in muscle HbO2 (P < 0.05), but not changes in cerebral HbO2 (P > 0.05) at all three intensities. Force output declined by 8% from the 1st to the 24th contraction only at 60% MVC and was accompanied by systematic increases in RMS, cerebral HbO2 and Hbtot with a leveling off in muscle HbO2 and Hbtot. These changes were independent of alterations in mean arterial pressure. Since cerebral blood flow and oxygenation were elevated at 60% MVC, we attribute the development of fatigue to reduced muscle oxygen availability rather than impaired central neuronal activation.