Arterial Pressure Oscillations Research Articles

Dynamic cerebral autoregulation quantification with spontaneous arterial blood pressure oscillations: Is transfer function analysis our best option?

Dynamic cerebral autoregulation quantification with spontaneous arterial blood pressure oscillations: Is transfer function analysis our best option?

The effect of oscillatory hemodynamics on the cardiovascular responses to simulated hemorrhage during isocapnia.

During cerebral hypoperfusion induced by lower body negative pressure (LBNP), cerebral tissue oxygenation is protected with oscillatory arterial pressure and cerebral blood flow at low frequencies (0.1 Hz and 0.05 Hz), despite no protection of cerebral blood flow or oxygen delivery. However, hypocapnia induced by LBNP contributes to cerebral blood flow reductions, and may mask potential protective effects of hemodynamic oscillations on cerebral blood flow. We hypothesized that under isocapnic conditions, forced oscillations of arterial pressure and blood flow at 0.1 Hz and 0.05 Hz would attenuate reductions in extra- and intracranial blood flow during simulated hemorrhage using LBNP. Eleven human participants underwent three LBNP profiles: a nonoscillatory condition (0 Hz) and two oscillatory conditions (0.1 Hz and 0.05 Hz). End-tidal (et) CO2 and etO2 were clamped at baseline values using dynamic end-tidal forcing. Cerebral tissue oxygenation (ScO2), internal carotid artery (ICA) blood flow, and middle cerebral artery velocity (MCAv) were measured. With clamped etCO2, neither ICA blood flow (ANOVA P = 0.93) nor MCAv (ANOVA P = 0.36) decreased with LBNP, and these responses did not differ between the three profiles (ICA blood flow: 0 Hz: 2.2 ± 5.4%, 0.1 Hz: -0.4 ± 6.6%, 0.05 Hz: 0.2 ± 4.8%; P = 0.56; MCAv: 0 Hz: -2.3 ± 7.8%, 0.1 Hz: -1.3 ± 6.1%, 0.05 Hz: -3.1 ± 5.0%; P = 0.87). Similarly, ScO2 did not decrease with LBNP (ANOVA P = 0.21) nor differ between the three profiles (0 Hz: -2.6 ± 3.3%, 0.1 Hz: -1.6 ± 1.5%, 0.05 Hz: -0.2 ± 2.8%; P = 0.13). Contrary to our hypothesis, cerebral blood flow and tissue oxygenation were protected during LBNP with isocapnia, regardless of whether hemodynamic oscillations were induced.NEW & NOTEWORTHY We examined the role of forcing oscillations in arterial pressure and blood flow at 0.1 Hz and 0.05 Hz on extra- and intracranial blood flow and cerebral tissue oxygenation during simulated hemorrhage (using lower body negative pressure, LBNP) under isocapnic conditions. Contrary to our hypothesis, both cerebral blood flow and cerebral tissue oxygenation were completely protected during simulated hemorrhage with isocapnia, regardless of whether oscillations in arterial pressure and cerebral blood flow were induced. These findings highlight the protective effect of preventing hypocapnia on cerebral blood flow under simulated hemorrhage conditions.

Conductivity reactivity index for monitoring of cerebrovascular autoregulation in early cerebral ischemic rabbits

BackgroundCerebrovascular autoregulation (CVAR) is the mechanism that maintains constant cerebral blood flow by adjusting the caliber of the cerebral vessels. It is important to have an effective, contactless way to monitor and assess CVAR in patients with ischemia.MethodsThe adjustment of cerebral blood flow leads to changes in the conductivity of the whole brain. Here, whole-brain conductivity measured by the magnetic induction phase shift method is a valuable alternative to cerebral blood volume for non-contact assessment of CVAR. Therefore, we proposed the correlation coefficient between spontaneous slow oscillations in arterial blood pressure and the corresponding magnetic induction phase shift as a novel index called the conductivity reactivity index (CRx). In comparison with the intracranial pressure reactivity index (PRx), the feasibility of the conductivity reactivity index to assess CVAR in the early phase of cerebral ischemia has been preliminarily confirmed in animal experiments.ResultsThere was a significant difference in the CRx between the cerebral ischemia group and the control group (p = 0.002). At the same time, there was a significant negative correlation between the CRx and the PRx (r = − 0.642, p = 0.002) after 40 min after ischemia. The Bland–Altman consistency analysis showed that the two indices were linearly related, with a minimal difference and high consistency in the early ischemic period. The sensitivity and specificity of CRx for cerebral ischemia identification were 75% and 20%, respectively, and the area under the ROC curve of CRx was 0.835 (SE = 0.084).ConclusionThe animal experimental results preliminarily demonstrated that the CRx can be used to monitor CVAR and identify CVAR injury in early ischemic conditions. The CRx has the potential to be used for contactless, global, bedside, and real-time assessment of CVAR of patients with ischemic stroke.

Hemodynamic responses to oscillatory thigh cuff inflations

Background. In the clinical setting, individuals have varying tolerance to hypovolemia induced by blood loss. Experimental generation of 0.1 Hz oscillations (~10-s cycle) in arterial pressure and cerebral blood flow via oscillatory lower body negative pressure (OLBNP) increases tolerance to this simulated hemorrhage, and protects cerebral tissue oxygenation. However, use of OLBNP as a method of inducing hemodynamic oscillations in the clinical setting is limited as: 1) it is a large and cumbersome technique, and; 2) it induces central hypovolemia, which would only worsen the magnitude of hemorrhage. In this study we evaluated a more clinically applicable method of inducing 0.1 Hz oscillations in arterial pressure and cerebral blood flow, using intermittent inflation of bilateral thigh cuffs. We hypothesized that the amplitude of arterial pressure and cerebral blood flow oscillations at 0.1 Hz would increase in response to repeated thigh cuff inflations at 0.1 Hz when compared with a baseline control condition. Methods. Ten healthy human subjects were tested (6 male, 4 female; 26.8 ± 4.1 y). Middle cerebral artery velocity (MCAv) was measured via transcranial doppler ultrasound, arterial pressure was measured via finger photoplethysmography, and end tidal CO2 (etCO2) was measured via capnography. Following a 10-min baseline period, intermittent thigh cuff inflations at 0.1 Hz and 230 mmHg (5-s inflation, 5-s deflation) were performed for 10-min (“oscillations”). 0.1 Hz oscillatory amplitude of mean arterial pressure and mean MCAv were quantified using Fast Fourier transformation during the last 5-min of baseline and the oscillatory period, and compared via two-tailed paired t-tests. Results. The amplitude of 0.1 Hz oscillations increased during the oscillatory period vs. baseline for mean arterial pressure (baseline: 1.7 ± 1.0 mmHg2 vs. oscillations: 9.0 ± 6.2 mmHg2; P = 0.004) and mean MCAv (baseline: 1.1 ± 0.6 (cm/s)2 vs. oscillations: 3.4 ± 3.1 (cm/s)2; P = 0.04). Absolute mean arterial pressure was similar between baseline and the oscillatory period (baseline: 97.2 ± 8.1 mmHg vs. oscillations: 99.1 ± 15.0 mmHg; P = 0.54), but absolute mean MCAv was lower during the oscillatory period (baseline: 61.7 ± 14.6 cm/s vs. oscillations: 53.2 ± 13.1 cm/s; P = 0.02). This reduction in mean MCAv was most likely due to hypocapnia (indexed by etCO2) induced by pacing the breathing of all subjects at ≥10 breaths/min (baseline: 33.2 ± 4.8 mmHg vs. oscillations 27.2 ± 4.5 mmHg; P = 0.005). Conclusions. Intermittent thigh cuff inflations at 0.1 Hz induced 0.1 Hz oscillations in both arterial pressure and cerebral blood flow when compared to baseline. These findings indicate that intermittent thigh cuff inflations could be developed as a method to induce pulsatile perfusion as a potential new therapy for individuals experiencing major blood loss. American Heart Association (Transformational Project Award) #19TPA34910073 and UNTHSC Physiology and Anatomy Seed Grant 2021 This is the full abstract presented at the American Physiology Summit 2023 meeting and is only available in HTML format. There are no additional versions or additional content available for this abstract. Physiology was not involved in the peer review process.

Induced Blood Flow Oscillations at 0.1 Hz Protects Oxygenation of Severely Ischemic Tissue

Background: Early interventions that improve vital organ perfusion will reduce the number of lives lost from blood loss injuries. We have shown that generating 10 second (~0.1 Hz) fluctuations or “oscillations” in arterial pressure and blood flow during simulated hemorrhage protects cerebral tissue oxygenation. Lower body negative pressure (LBNP) was used to both simulate hemorrhage, and induce the hemodynamic oscillations in these previous studies. However, the magnitude of cerebral tissue ischemia is limited to 20-30% with LBNP due to the onset of pre-syncopal symptoms. To examine the effect of 0.1 Hz hemodynamic oscillations on blood flow delivery and tissue oxygenation of severely ischemic tissues, we developed a limb ischemia model. Hypothesis: Oscillatory arterial pressure and blood flow will attenuate reductions in brachial artery blood flow and forearm tissue oxygenation in a severely ischemic limb. Methods: Nine healthy human subjects (5M, 4F; 27.2 ± 4.1 y) completed two experimental protocols separated by ≥48 h. In both conditions, ischemia of the forearm was induced with a pneumatic cuff on the upper arm to decrease brachial artery (BA) blood velocity by ~70-80% from baseline. In the oscillation condition (OSC), 0.1 Hz oscillations in mean arterial pressure (MAP) and BA blood flow were then induced by inflating and deflating bilateral thigh cuffs every 10 seconds (0.1 Hz) throughout the forearm ischemia period. In the control condition (CON), the thigh cuffs were in place, but were inactive throughout the forearm ischemia period. BA blood flow was measured via duplex ultrasound, forearm muscle tissue oxygenation (SmO2) was measured via near infrared spectroscopy, and arterial pressure was measured via finger photoplethysmography. Results: The magnitude of forearm ischemia, indexed by the reduction in BA blood velocity, was matched between protocols (CON: -75.2 ± 8.4 % vs. OSC: -78.3 ± 7.8 %, p=0.20). Power spectral density of 0.1 Hz oscillations in MAP (CON: 19.4 ± 22.8 mmHg2 vs. OSC: 716.8 ± 514.6 mmHg2; p<0.001) and BA blood velocity (CON: 0.7 ± 1.0 cm/s2 vs. OSC: 10.6 ± 7.1 cm/s2, p=0.02) were greater with oscillatory thigh cuff compression compared with the control condition. While oscillatory thigh cuff compression during forearm ischemia had no effect on absolute MAP (CON: 94.3 ± 6.6 mmHg vs. OSC: 94.4 ± 10.8 mmHg, p=0.99), BA blood flow (CON: 9.7 ± 5.8 ml/min vs. OSC: 9.5 ± 7.3 ml/min, p=0.82), or BA conductance (CON: 0.10 ± 0.06 ml/min/mmHg vs. OSC: 0.09 ± 0.06 ml/min/mmHg, p=0.39), the reduction in SmO2 was attenuated (CON: -38.7 ± 8.3 % vs. OSC: -28.4 ± 9.7 %; p=0.04). These data provide further evidence for the use of 0.1 Hz hemodynamic oscillations as a therapeutic intervention for conditions associated with severe vital organ ischemia such as hemorrhage, stroke, myocardial infarction, and sepsis. National Institutes of Health/National Institute on Aging T32 Ruth Kirschstein Institutional National Research Service Award (T32AG020494); American Heart Association Transformational Project Award (19TPA34910073) This is the full abstract presented at the American Physiology Summit 2023 meeting and is only available in HTML format. There are no additional versions or additional content available for this abstract. Physiology was not involved in the peer review process.

Dynamic cerebral autoregulation measured by diffuse correlation spectroscopy

Dynamic cerebral autoregulation (dCA) can be derived from spontaneous oscillations in arterial blood pressure (ABP) and cerebral blood flow (CBF). Transcranial Doppler (TCD) measures CBF-velocity and is commonly used to assess dCA. Diffuse correlation spectroscopy (DCS) is a promising optical technique for non-invasive CBF monitoring, so here we aimed to validate DCS as a tool for quantifying dCA. In 33 healthy adults and 17 acute ischemic stroke patients, resting-state hemodynamic were monitored simultaneously with high-speed (20 Hz) DCS and TCD. dCA parameters were calcaulated by a transfer function analysis using a Fourier decomposition of ABP and CBF (or CBF-velocity). Strong correlation was found between DCS and TCD measured gain (magnitude of regulation) in healthy volunteers (r = 0.73, p < 0.001) and stroke patients (r = 0.76, p = 0.003). DCS-gain retained strong test-retest reliability in both groups (ICC 0.87 and 0.82, respectively). DCS and TCD-derived phase (latency of regulation) did not significantly correlate in healthy volunteers (r = 0.12, p = 0.50) but moderately correlated in stroke patients (r = 0.65, p = 0.006). DCS-derived phase was reproducible in both groups (ICC 0.88 and 0.90, respectively). High-frequency DCS is a promising non-invasive bedside technique that can be leveraged to quantify dCA from resting-state data, but the discrepancy between TCD and DCS-derived phase requires further investigation.

Coherent Spontaneous Hemodynamics in the Human Brain

<italic xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:xlink="http://www.w3.org/1999/xlink">Goal:</i> This work investigates the presence of cerebral hemodynamics (namely Oxy (O) and Deoxy (D) hemoglobin concentrations) that are coherent with spontaneous oscillations in Arterial Blood Pressure (ABP) in 78 healthy subjects during a driving simulation task. <italic xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:xlink="http://www.w3.org/1999/xlink">Methods:</i> Spatially resolved O and D were measured on the prefrontal cortex with multi-channel near-infrared spectroscopy (NIRS). Wavelet coherence and phasor analysis were performed between O and ABP, and between D and ABP to evaluate the amplitude ratio, phase difference, and duration of significant coherence. <italic xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:xlink="http://www.w3.org/1999/xlink">Results</i> : In the low-frequency range, oscillations at 0.1 Hz featured significant coherence for the longest time fraction (∼10%-30%). At this frequency, the amplitude ratio and phase difference showed a greater variance across subjects than over cortical locations, and no significant difference between driving tasks and baseline. <italic xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:xlink="http://www.w3.org/1999/xlink">Conclusions</i> : Measuring low-frequency cerebral hemodynamics that are coherent with systemic ABP holds promise for non-invasive assessment of cerebral perfusion and autoregulation at the cerebral microvascular level.

The potential therapeutic benefits of low frequency haemodynamic oscillations.

Haemodynamic oscillations occurring at frequencies below the rate of respiration have been observed experimentally for more than a century. Much of the research regarding these oscillations, observed in arterial pressure and blood flow, has focused on mechanisms of generation and methods of quantification. However, examination of the physiological role of these oscillations has been limited. Multiple studies have demonstrated that oscillations in arterial pressure and blood flow are associated with the protection in tissue oxygenation or functional capillary density during conditions of reduced tissue perfusion. There is also evidence that oscillatory blood flow can improve clearance of interstitial fluid, with a growing number of studies demonstrating a role for oscillatory blood flow to aid in clearance of debris from the brain. The therapeutic potential of these haemodynamic oscillations is an important new area of research which may have beneficial impact in treating conditions such as stroke, cardiac arrest, blood loss injuries, sepsis, or even Alzheimer's disease and vascular dementia.

Inducing oscillations in positive end-expiratory pressure improves assessment of cerebrovascular pressure reactivity in patients with traumatic brain injury.

The cerebral pressure reactivity index (PRx), through intracranial pressure (ICP) measurements, informs clinicians about the cerebral autoregulation (CA) status in adult-sedated patients with traumatic brain injury (TBI). Using PRx in clinical practice is currently limited by variability over shorter monitoring periods. We applied an innovative method to reduce the PRx variability by ventilator-induced slow (1/min) positive end-expiratory pressure (PEEP) oscillations. We hypothesized that, as seen in a previous animal model, the PRx variability would be reduced by inducing slow arterial blood pressure (ABP) and ICP oscillations without other clinically relevant physiological changes. Patients with TBI were ventilated with a static PEEP for 30 min (PRx period) followed by a 30-min period of slow [1/min (0.0167 Hz)] +5 cmH2O PEEP oscillations (induced (iPRx period). Ten patients with TBI were included. No clinical monitoring was discontinued and no additional interventions were required during the iPRx period. The PRx variability [measured as the standard deviation (SD) of PRx] decreased significantly during the iPRx period from 0.25 (0.22-0.30) to 0.14 (0.09-0.17) (P = 0.006). There was a power increase around the induced frequency (1/min) for both ABP and ICP (P = 0.002). In conclusion, 1/min PEEP-induced oscillations reduced the PRx variability in patients with TBI with ICP levels <22 mmHg. No other clinically relevant physiological changes were observed. Reduced PRx variability might improve CA-guided perfusion management by reducing the time to find "optimal" perfusion pressure targets. Larger studies with prolonged periods of PEEP-induced oscillations are required to take it to routine use.NEW & NOTEWORTHY Cerebral autoregulation assessment requires sufficient slow arterial blood pressure (ABP) waves. However, spontaneous ABP waves may be insufficient for reliable cerebral autoregulation estimations. Therefore, we applied a ventilator "sigh-function" to generate positive end-expiratory pressure oscillations that induce slow ABP waves. This method demonstrated a reduced variability of the pressure reactivity index, commonly used as continuous cerebral autoregulation measure in a traumatic brain injury population.

Influence of high‐intensity interval training to exhaustion on the directional sensitivity of the cerebral pressure‐flow relationship in young endurance‐trained men

We previously reported subtle dynamic cerebral autoregulation (dCA) alterations following 6 weeks of high‐intensity interval training (HIIT) to exhaustion using transfer function analysis (TFA) on forced mean arterial pressure (MAP) oscillations in young endurance‐trained men. However, accumulating evidence suggests the cerebrovasculature better buffers cerebral blood flow changes when MAP acutely increases compared to when MAP acutely decreases. Whether HIIT affects the directional sensitivity of the cerebral pressure‐flow relationship in these athletes is unknown. In 18 endurance‐trained men (age: 27 ± 6 years, VO2max: 55.5 ± 4.7 ml·kg−1·min−1), we evaluated the impact of 6 weeks of HIIT to exhaustion on dCA directionality using induced MAP oscillations during 5‐min 0.05 and 0.10 Hz repeated squat‐stands. We calculated time‐adjusted changes in middle cerebral artery mean blood velocity (MCAv) per change in MAP (ΔMCAvT/ΔMAPT) for each squat transition. Then, we compared averaged ΔMCAvT/ΔMAPT during MAP increases and decreases. Before HIIT, ΔMCAvT/ΔMAPT was comparable between MAP increases and decreases during 0.05 Hz repeated squat‐stands (p = 0.518). During 0.10 Hz repeated squat‐stands, ΔMCAvT/ΔMAPT was lower during MAP increases versus decreases (0.87 ± 0.17 vs. 0.99 ± 0.23 cm·s−1·mmHg−1, p = 0.030). Following HIIT, ΔMCAvT/ΔMAPT was superior during MAP increases over decreases during 0.05 Hz repeated squat‐stands (0.97 ± 0.38 vs. 0.77 ± 0.35 cm·s−1·mmHg−1, p = 0.002). During 0.10 Hz repeated squat‐stands, dCA directional sensitivity disappeared (p = 0.359). These results suggest the potential for HIIT to influence the directional sensitivity of the cerebral pressure‐flow relationship in young endurance‐trained men.

Effects of Sustained Hypobaric Hypoxia on Amplitude of Forced Hemodynamic Oscillations During Central Hypovolemia

IntroductionForcing oscillations in arterial pressure and cerebral blood flow at 0.1 Hz during simulated hemorrhage protects cerebral oxygenation at both low and high altitude. Arterial pressure oscillations at 0.1 Hz are endogenously driven by rhythmic fluctuations in sympathetic nerve activity. As hypobaric hypoxia increases basal sympathetic activity, we hypothesize that the amplitude of forced oscillations in arterial pressure and cerebral blood flow during simulated hemorrhage will be greater at high altitude compared to low altitude.Methods8 healthy human participants (4 M, 24.7 ± 4.1 y; 4 F, 34.3 ± 8.3 y) underwent a hypovolemic oscillatory lower body negative pressure (OLBNP) protocol, where chamber pressure reduced to ‐60 mmHg then oscillated every 5‐s between ‐30 mmHg and ‐90 mmHg over 10‐min (0.1 Hz). This protocol was performed at both low altitude (LA; Calgary, Alberta, Canada; 1045 m) and high altitude (HA; White Mountain, California, USA; 3800 m). Mean arterial pressure (MAP), mean middle cerebral artery velocity (MCAv), and cerebral tissue oxygenation (ScO2) were recorded continuously. Frequency analysis (via continuous wavelet transform) was used to quantify oscillations in MAP and mean MCAv at ~0.1 Hz. Data were analyzed with linear mixed‐models and paired t‐tests. All data are represented as mean ± SD.ResultsBaseline amplitude of oscillations were similar between HA and LA for MAP (1.9 ± 0.6 mmHg vs. 1.2 ± 0.5 mmHg; P = 0.47) and mean MCAv (0.9 ± 0.4 cm/s vs. 1.1 ± 0.3 cm/s; P = 0.91). Oscillatory amplitudes increased with 0.1 Hz OLBNP and altitude for MAP (ANOVA main effect, OLBNP: P &lt; 0.001, Altitude: P = 0.007) and mean MCAv (ANOVA main effect, OLBNP: P = 0.002, Altitude: P = 0.008). Amplitude of oscillations during OLBNP were greater at HA for both MAP (4.0 ± 2.1 mmHgvs. 2.6 ± 1.4 mmHg, P = 0.05) and mean MCAv (2.4 ± 1.1 cm/svs. 0.9 ± 0.4 cm/s; P = 0.01). The relative (%∆) decrease in ScO2 was not different between HA and LA (‐0.63 ± 0.92 % vs. ‐2.56 ± 2.61 %, P = 0.11).ConclusionsOscillatory amplitudes at 0.1 Hz in both MAP and mean MCAv increased during OLBNP at high altitude. This effect may be due, in part, to the sympathoexcitatory stimulus of hypobaric hypoxia, and does not alter the protection of cerebral tissue oxygenation in this environment.

The Effect of Unilateral Nephrectomy on Arterial Blood Pressure Variability in Spontaneously Hypertensive Rats

&#x0D; &#x0D; &#x0D; The aim of the current study was to investigate the effects of unilateral nephrectomy (ULN) on fast oscillation of arterial blood pressure in spontaneously hypertensive rats (SHR). Experiments were carried out on conscious normotensive Wistar rats and SHR divided in groups with intact kidneys: W, n = 10; SHR, n = 9 and with unilateral nephrectomy: WN, n = 10; SHRN, n = 10. ULN was performed under general anaesthesia (Nembutal 35 mg/kg b.w. i.p.), eight days before the experiments. Blood pressure variability was investigated by means of spectral analysis of systolic (SAP) diastolic (DAP) and mean (MAP) arterial blood pressure, estimated in directly registered arterial blood pressure wave. In SAP, DAP and MAP spectrograms, derived by Lab View software equipment, the spectral power (P) in low (LF, 20–195 mHz), mid (MF, 195–605 mHz) and high frequency (HF, 605—3000 mHz) bands was calculated. PLF in SAP spectrograms increased after ULN both in Wistar rats and SHR. ULN led to decrease of PMF in SAP, DAP and MAP spectrograms only in SHR. The ULN provokes changes in blood pressure variability in different manner in the normotensive and the spontaneously hypertensive rats. In addition to humorally-mediated low-frequency oscillations, ULN in SHR also af- fected the spectral characteristics of the arterial pressure in which sympathetic nervous activity operates.&#x0D; &#x0D; &#x0D;

Characterization of Mayer-wave oscillations in functional near-infrared spectroscopy using a physiologically informed model of the neural power spectra.

.Significance: Mayer waves are spontaneous oscillations in arterial blood pressure that can mask cortical hemodynamic responses associated with neural activity of interest.Aim: We aim to characterize the properties of oscillations in the functional near-infrared spectroscopy (fNIRS) signal generated by Mayer waves in a large sample of fNIRS recordings. Further, we aim to determine the impact of short-channel correction for the attenuation of these unwanted signal components.Approach: Mayer-wave oscillation parameters were extracted from 310 fNIRS measurements using the fitting oscillations and one-over-f method to compute normative values. The effect of short-channel correction on Mayer-wave oscillation power was quantified on 222 measurements. The practical benefit of the short-channel correction approach for reducing Mayer waves and improving response detection was also evaluated on a subgroup of 17 fNIRS measurements collected during a passive auditory speech detection experiment.Results: Mayer-wave oscillations had a mean frequency of 0.108 Hz, bandwidth of 0.04 Hz, and power of . The distribution of oscillation signal power was positively skewed, with some measurements containing large Mayer waves. Short-channel correction significantly reduced the amplitude of these undesired signals; greater attenuation was observed for measurements containing larger Mayer-wave oscillations.Conclusions: A robust method for quantifying Mayer-wave oscillations in the fNIRS signal spectrum was presented and used to provide normative parameterization. Short-channel correction is recommended as an approach for attenuating Mayer waves, particularly in participants with large oscillations.

The Influence of Carbon Dioxide on Cerebral Autoregulation During Sevoflurane-based Anesthesia in Patients With Type 2 Diabetes.

Cerebral autoregulation (CA) continuously adjusts cerebrovascular resistance to maintain cerebral blood flow (CBF) constant despite changes in blood pressure. Also, CBF is proportional to changes in arterial carbon dioxide (CO 2 ) (cerebrovascular CO 2 reactivity). Hypercapnia elicits cerebral vasodilation that attenuates CA efficacy, while hypocapnia produces cerebral vasoconstriction that enhances CA efficacy. In this study, we quantified the influence of sevoflurane anesthesia on CO 2 reactivity and the CA-CO 2 relationship. We studied patients with type 2 diabetes mellitus (DM), prone to cerebrovascular disease, and compared them to control subjects. In 33 patients (19 DM, 14 control), end-tidal CO 2 , blood pressure, and CBF velocity were monitored awake and during sevoflurane-based anesthesia. CA, calculated with transfer function analysis assessing phase lead (degrees) between low-frequency oscillations in CBF velocity and mean arterial blood pressure, was quantified during hypocapnia, normocapnia, and hypercapnia. In both control and DM patients, awake CO 2 reactivity was smaller (2.8%/mm Hg CO 2 ) than during sevoflurane anesthesia (3.9%/mm Hg; P <0.005). Hyperventilation increased CA efficacy more (3 deg./mm Hg CO 2 ) in controls than in DM patients (1.8 deg./mm Hg CO 2 ; P <0.001) in both awake and sevoflurane-anesthetized states. The CA-CO 2 relationship is impaired in awake patients with type 2 DM. Sevoflurane-based anesthesia does not further impair this relationship. In patients with DM, hypocapnia induces cerebral vasoconstriction, but CA efficacy does not improve as observed in healthy subjects.

Peaks and valleys: oscillatory cerebral blood flow at high altitude protects cerebral tissue oxygenation

Introduction. Oscillatory patterns in arterial pressure and blood flow (at ∼0.1 Hz) may protect tissue oxygenation during conditions of reduced cerebral perfusion and/or hypoxia. We hypothesized that inducing oscillations in arterial pressure and cerebral blood flow at 0.1 Hz would protect cerebral blood flow and cerebral tissue oxygen saturation during exposure to a combination of simulated hemorrhage and sustained hypobaric hypoxia. Methods. Eight healthy human subjects (4 male, 4 female; 30.1 ± 7.6 year) participated in two experiments at high altitude (White Mountain, California, USA; altitude, 3800 m) following rapid ascent and 5–7 d of acclimatization: (1) static lower body negative pressure (LBNP, control condition) was used to induce central hypovolemia by reducing chamber pressure to −60 mmHg for 10 min (0 Hz), and; (2) oscillatory LBNP where chamber pressure was reduced to −60 mmHg, then oscillated every 5 s between −30 mmHg and −90 mmHg for 10 min (0.1 Hz). Measurements included arterial pressure, internal carotid artery (ICA) blood flow, middle cerebral artery velocity (MCAv), and cerebral tissue oxygen saturation (ScO2). Results. Forced 0.1 Hz oscillations in mean arterial pressure and mean MCAv were accompanied by a protection of ScO2 (0.1 Hz: −0.67% ± 1.0%; 0 Hz: −4.07% ± 2.0%; P = 0.01). However, the 0.1 Hz profile did not protect against reductions in ICA blood flow (0.1 Hz: −32.5% ± 4.5%; 0 Hz: −19.9% ± 8.9%; P = 0.24) or mean MCAv (0.1 Hz: −18.5% ± 3.4%; 0 Hz: −15.3% ± 5.4%; P = 0.16). Conclusions. Induced oscillatory arterial pressure and cerebral blood flow led to protection of ScO2 during combined simulated hemorrhage and sustained hypoxia. This protection was not associated with the preservation of cerebral blood flow suggesting preservation of ScO2 may be due to mechanisms occurring within the microvasculature.

Time‐Frequency Analysis of Hemodynamics Oscillations during Presyncopal Lower Body Negative Pressure (LBNP)

Introduction Greater low frequency (LF) oscillations (~0.1 Hz) in mean arterial pressure (MAP) and cerebral blood flow (indexed by middle cerebral artery velocity; MCAv) have been associated with higher tolerance to central hypovolemia. As the fast Fourier transform approach was used in these prior studies, measuring exact timing of oscillatory amplitude was not possible. In the present study, the continuous wavelet transform was used for time localization and measurement of the magnitude of LF oscillations during application of lower body negative pressure (LBNP) to presyncope to reduce cerebral perfusion. We hypothesized that the magnitude of LF oscillations in MAP and MCAv would be higher in subjects with greater tolerance to this stress. We also hypothesized that the time of instantaneous maximum magnitude of LF oscillations would be further from baseline for high tolerant subjects. Methods 31 healthy human subjects (14 F: 17 M; 25.1 ± 3.0 y) underwent a stepwise LBNP protocol to presyncope. Subjects were classified as high tolerant (HT) if they completed the -60 mmHg stage of LBNP, and low tolerant (LT) if they did not. Continuous beat-to-beat MAP and mean MCAv were recorded. The continuous wavelet transform was used to extract magnitude of oscillations within the LF range (0.07-0.15 Hz) over time for both MAP and mean MCAv. The instantaneous maximum magnitude of LF oscillations was then extracted. Pearson's correlation was calculated for instantaneous LF magnitude of MAP and mean MCAv versus presyncopal time. A t-test was then used to compare magnitude and relative time of LF oscillations between HT and LT subjects. Results The maximum magnitude of MAP LF oscillations was positively correlated with presyncopal time (R = 0.39, P = 0.03). The maximum magnitude of MCAv LF oscillations, however, was not correlated with presyncopal time (R = -0.03, P = 0.86). When assessing HT and LT subjects, no differences were observed for maximum magnitude of LF oscillations in MAP (HT 4.3 ± 1.0, LT 3.7 ± 1.2, P=0.15) or MCAv (HT 3.1 ± 0.9, LT 3.1 ± 0.7, P=0.91). Time to maximum magnitude of LF oscillations was greater in high tolerant subjects for both MAP (HT 1384.5 ± 329.6 s, LT 798.6 ± 416.8 s, P<0.01) and MCAv (HT 1064.3 ± 431.6 s, LT 662.4 ± 380.1 s, P=0.01). When expressing the time of maximum amplitude as a percent of presyncopal time, the average time in all subjects for MAP was 73.6 ± 22.0 % and 59.6 ± 26.1 % for MCAv, and there were no differences between tolerance groups in either MAP (HT 79.5 ± 14.0 %, LT 67.4 ± 27.3 %, P=0.14) or MCAv (HT 61.8 ± 24.8 %, LT 57.3 ± 28.1 %, P=0.64). Conclusions Using wavelet analysis, only the maximum magnitude of MAP LF oscillations was modestly correlated to presyncopal time. Contrary to previous measures using fast Fourier transform, there was no difference in instantaneous maximum magnitude of oscillations in MAP and mean MCAv between high and low tolerant subjects indicating that both groups could mount similar responses. Interestingly, the relative timing of maximum magnitude of oscillations in MAP and MCAv was no different between tolerance groups.

Blood pressure drives multispectral tuning of inspiration via a linked-loop neural network.

The respiratory motor pattern is coordinated with cardiovascular system regulation. Inspiratory drive and respiratory phase durations are tuned by blood pressure and baroreceptor reflexes. We hypothesized that perturbations of systemic arterial blood pressure modulate inspiratory drive through a raphe-pontomedullary network. In 15 adult decerebrate vagotomized neuromuscular-blocked cats, we used multielectrode arrays to record the activities of 704 neurons within the medullary ventral respiratory column, pons, and raphe areas during baroreceptor-evoked perturbations of breathing, as measured by altered peak activity in integrated efferent phrenic nerve activity and changes in respiratory phase durations. Blood pressure was transiently (30 s) elevated or reduced by inflations of an embolectomy catheter in the descending aorta or inferior vena cava. S-transform time-frequency representations were calculated for multiunit phrenic nerve activity and some spike trains to identify changes in rhythmic activity during perturbations. Altered firing rates in response to either or both conditions were detected for 474 of 704 tested cells. Spike trains of 17,805 neuron pairs were evaluated for short-time scale correlational signatures indicative of functional connectivity with standard cross-correlation analysis, supplemented with gravitational clustering; ∼70% of tested (498 of 704) and responding neurons (333 of 474) were involved in a functional correlation with at least one other cell. Changes in high-frequency oscillations in the spiking of inspiratory neurons and the evocation or resetting of slow quasi-periodic fluctuations in the respiratory motor pattern associated with oscillations of arterial pressure were observed. The results support a linked-loop pontomedullary network architecture for multispectral tuning of inspiration.NEW & NOTEWORTHY The brain network that supports cardiorespiratory coupling remains poorly understood. Using multielectrode arrays, we tested the hypothesis that blood pressure and baroreceptor reflexes "tune" the breathing motor pattern via a raphe-pontomedullary network. Neuron responses to changes in arterial pressure and identified functional connectivity, together with altered high frequency and slow Lundberg B-wave oscillations, support a model with linked recurrent inhibitory loops that stabilize the respiratory network and provide a path for transmission of baroreceptor signals.

Diffuse optical assessment of cerebral-autoregulation in older adults stratified by cerebrovascular risk.

Diagnosis of cerebrovascular disease (CVD) at early stages is essential for preventing sequential complications. CVD is often associated with abnormal cerebral microvasculature, which may impact cerebral-autoregulation (CA). A novel hybrid near-infrared diffuse optical instrument and a finger plethysmograph were used to simultaneously detect low-frequency oscillations (LFOs) of cerebral blood flow (CBF), oxy-hemoglobin concentration ([HbO2 ]), deoxy-hemoglobin concentration ([Hb]) and mean arterial pressure (MAP) in older adults before, during and after 70° head-up-tilting (HUT). The participants with valid data were divided based on Framingham risk score (FRS, 1-30 points) into low-risk (FRS ≤15, n = 13) and high-risk (FRS >15, n = 11) groups for developing CVD. The LFO gains were determined by transfer function analyses with MAP as the input, and CBF, [HbO2 ] and [Hb] as the outputs (CA ∝ 1/Gain). At resting-baseline, LFO gains in the high-risk group were relatively lower compared to the low-risk group. The lower baseline gains in the high-risk group may attribute to compensatory mechanisms to maintain stronger steady-state CAs. However, HUT resulted in smaller gain reductions in the high-risk group compared to the low-risk group, suggesting weaker dynamic CAs. LFO gains are potentially valuable biomarkers for early detection of CVD based on associations with CAs.

Impact Of 6-month Exercise Training On Cerebrovascular Function In Persons With Spinal Cord Injury

Persons with spinal cord injury (SCI) have a four-fold greater risk for cerebrovascular disease, suggesting that they cannot maintain steady cerebral perfusion. While disruption in autonomic control after SCI may impact cerebral vascular function, chronic physical deconditioning may also play a substantial role. If so, full-body aerobic exercise may improve cerebrovascular function in persons with SCI. PURPOSE: To assess the impact of injury and habitual, whole-body functional electric stimulation (FES)-assisted aerobic exercise training on cerebrovascular function in persons with SCI. METHODS: Baseline hemodynamic (heart rate, blood pressure, CO2) and cerebral blood flow (CBF) responses to oscillations in arterial blood pressure via low-resistance breathing (i.e. autoregulation) and progressive increases in arterial CO2 via rebreathing (i.e. vasoreactivity) were measured in 16 able-bodied controls and 30 participants with SCI (n= 15 cervical and n = 15 thoracic). Nineteen participants with SCI (n= 9 cervical and n = 10 thoracic) completed 6-months of a FES-assisted rowing exercise training program. Changes in autoregulatory function, vasoreactivity, and VO2max were compared before and after aerobic exercise training via linear mixed effect model. RESULTS: Individuals with higher level SCI had slightly lower hemodynamic variables in comparison to able-bodied and those with lower level SCI and able-bodied. Greater VO2max was related to increased vasoreactivity (R2=0.45, p<0.01) at baseline. Overall, VO2max increased significantly after training (p<0.01). Vasoreactivity also tended to increase with training, but the change was not statistically significant due to high variability. Given this, we assessed the relation between the change in VO2max and vasoreactivity in exercise “responders,” defined as those with >10% change in VO2max; n=8. In responders, an increase in VO2max was strongly associated with an increase in vasoreactivity (R2=0.72, p<.01) regardless of the level of SCI. CONCLUSION: Cerebral vasoreactivity is impaired in individuals with SCI. This impairment is primarily due to physical deconditioning, and can be improved by habitual aerobic exercise.

Compromised Dynamic Cerebral Autoregulation in Patients With Idiopathic Rapid Eye Movement Behavior Disorder: A Case-Control Study Using Transcranial Doppler.

BackgroundPatients with idiopathic rapid eye movement behavior disorder (IRBD) have been suggested to exhibit altered cerebral perfusion and abnormal cerebral blood flow, which imply a possibility of cerebral autoregulation (CA) impairment. We aimed to investigate the dynamic CA (dCA) in patients with IRBD during wakefulness and to explore the correlations between dCA parameters and clinical measurements.MethodsWe assessed the dCA capability of 30 patients with IRBD and 36 sex- and age-matched healthy controls by using transcranial Doppler and finger plethysmography. CA function was evaluated by transfer function analysis based on spontaneous oscillation of cerebral blood flow and arterial blood pressure. Transfer function parameters (phase difference and gain) were used to quantify the CA.ResultsNo significant differences were observed between the right and left middle cerebral artery dCA parameters (phase difference and gain) of both groups. Patients with IRBD had significantly lower phase difference than the healthy controls, indicating their impaired CA capability. Besides, the value of gain in patients with IRBD was higher than the healthy controls, but the difference did not reach statistical level.ConclusionsCA function is compromised in patients with IRBD during wakefulness, which might be an intermediate link between IRBD and neurological symptoms.