Arterial Blood Pressure Fluctuations Research Articles

The cerebovasculature: a smooth (muscle) operator?

The cerebovasculature: a smooth (muscle) operator?

Cerebrovascular hemodynamic changes in multiple sclerosis patients during head-up tilt table test: effect of high-dose intravenous steroid treatment

Demyelination in multiple sclerosis (MS) may cause damage to the vegetative nervous system. Our objective was to examine cerebral autoregulation assessed via blood pressure and cerebral blood flow velocity fluctuations during head-up tilt table testing. We also investigated the effects of high-dose intravenous corticosteroid treatment. Transcranial Doppler registration of middle cerebral artery blood flow velocity and continuous blood pressure and heart rate monitoring were performed at rest and during tilt table testing in 30 MS patients. Ten age-matched healthy subjects were also examined as controls. Correlations between mean arterial blood pressure (MBP) and cerebral blood flow velocity (CBF) fluctuations were averaged, yielding the correlation coefficient index Mx. For a subgroup of 11 patients with acute exacerbations, results were also evaluated before and after methylprednisolone treatment (1 g/day intravenously for 5 days). No significant differences in the autoregulatory indices were seen between patients and controls, or between pre- and post-steroid results. Modeling CBF velocity changes associated with a 1-mmHg increase in MBP, significant differences (p < 0.05) were detected in patients vs. controls, and also after vs. before steroid administration. We conclude that cerebrovascular autoregulation impairments are detectable in early phase MS. Corticosteroid treatment has a significant effect on hemodynamic changes in acute exacerbations.

MRI study of cerebral, retinal and choroidal blood flow responses to acute hypertension

Blood flow (BF) in many tissues is stable during significant fluctuations in systemic arterial blood pressure or perfusion pressure under normal conditions. The regulatory mechanisms responsible for this non-passive BF behavior include both local and neural control mechanisms. This study evaluated cerebral BF (CBF), retinal BF (RBF) and choroidal BF (ChBF) responses to acute blood pressure increases in rats using magnetic resonance imaging (MRI). A transient increase in blood pressure inside the MRI scanner was achieved by mechanically inflating a balloon catheter to occlude the descending aorta near the diaphragm. We verified the rat model of mechanical occlusion and MRI approach by first measuring blood-flow regulatory responses to changing BP in the brain under normoxia and hypercapnia where the phenomenon is well documented. Retinal and choroidal blood-flow responses to transient increased arterial pressure were then investigated. In response to an acute increase in blood pressure, RBF exhibited autoregulatory behavior and ChBF exhibited baroregulation similar to that seen in the cerebral circulation. This approach may prove useful to investigate retinal and choroidal vascular dysregulation in rat models of retinal diseases with suspected vascular etiology.

Abstract 55: Prediction of Delayed Cerebral Ischemia After Subarachnoid Hemorrhage Using Variations of Dynamic Cerebral Autoregulation

The risk of delayed cerebral ischemia (DCI) after cerebral aneurysm rupture is increased in patients with large cerebral artery vasospasm (VS). The predictive value of VS is, however, far to be optimal. Assessment of cerebral microcirculation impairment using dynamic cerebral autoregulation (DCA) measurement might improve our ability to predict DCI in these patients. Methods. We included consecutive patients with low-grade aneurysmal subarachnoid hemorrhage (SAH) (WFNS 1 to 3) within 4 days of aneurysm rupture. DCA was evaluated using the moving correlation coefficient Mx calculated from spontaneous fluctuations of cerebral blood flow velocities and arterial blood pressure. Impairment of DCA was defined as Mx ≥ 0.3. Transcranial colour-coded sonography was performed every 48 hours to look for VS. Diagnosis of VS was based on a Lindegaard ratio &gt;3 (MCA), or mean flow velocities &gt; 130 cm/s (ACA). DCI was defined as neurologic deterioration caused by brain ischemia confirmed by brain imaging. Results. Thirty patients (19 women; mean age ± SD: 44.7 ± 12.1 years) were included. Twenty (66.7%) patients had VS. DCI occurred in six (20%) patients after a median delay of 10 days (range 8 to 13 days). Mx (mean ± SD) was heightened at baseline (0.43 ± 0.2) and at day 7 (0.46 ± 0.2), then decreased at day 14 (0.37 ± 0.18 (p = 0.034). Isolated measures of VS and Mx were not associated with DCI. However, the elevation of Mx between baseline and day 7 in patients with VS was predictive of subsequent DCI (positive likelihood ratio=5.01; negative likelihood ratio=0.19; P=0.005). Conclusion. Findings suggest that DCA assessment may help to predict better the risk of DCI after cerebral aneurysm rupture than the simple recordings of mean flow velocities.

Interindividual relationships between blood pressure and cerebral blood flow variability with intact and blunted cerebrovascular control

The relationships between blood pressure variability (BPV) and cerebral blood flow variability (CFV) across individuals in the presence of intact and blunted cerebrovascular control are poorly understood. This study sought to characterize the interindividual associations between spontaneous BPV and CFV under conditions of normal and blunted [calcium channel blockade (CCB)] cerebrovascular control in healthy humans. We analyzed blood pressure and flow velocity data from 12 subjects treated with CCB (60 mg oral nimodipine) and 11 subjects treated with a placebo pill. Spontaneously occurring fluctuations in mean arterial blood pressure (MAP) and middle cerebral artery flow velocity (MCAv(mean); transcranial Doppler) were characterized using power spectral and transfer function analysis in the very-low- (0.02-0.07 Hz), low- (0.07-0.20 Hz), and high-frequency (0.20-0.40 Hz) ranges. Across our study sample, MAP and MCAv(mean) power were positively correlated in all three frequency ranges, both before (R(2) = 0.34-0.67, all P < 0.01) and after CCB (R(2) = 0.53-0.61, all P < 0.02). Compared with placebo, CCB reduced very-low-frequency MAP (P < 0.05) and MCAv(mean) power (P < 0.01) and the low-frequency cross-spectral phase angle (P < 0.05). The magnitude of change in MAP and MCAv(mean) power with CCB (i.e., change scores) was positively related in the very-low-frequency range. Collectively, these findings indicate that CFV may be an explanatory factor in the association between elevated BPV and adverse cerebrovascular outcomes and support the possibility of using CCB to improve hemodynamic stability under resting conditions.

Detection of Impaired Cerebral Autoregulation Improves by Increasing Arterial Blood Pressure Variability

Although the assessment of dynamic cerebral autoregulation (CA) based on measurements of spontaneous fluctuations in arterial blood pressure (ABP) and cerebral blood flow (CBF) is a convenient and much used method, there remains uncertainty about its reliability. We tested the effects of increasing ABP variability, provoked by a modification of the thigh cuff method, on the ability of the autoregulation index to discriminate between normal and impaired CA, using hypercapnia as a surrogate for dynamic CA impairment. In 30 healthy volunteers, ABP (Finapres) and CBF velocity (CBFV, transcranial Doppler) were recorded at rest and during 5% CO(2) breathing, with and without pseudo-random sequence inflation and deflation of bilateral thigh cuffs. The application of thigh cuffs increased ABP and CBFV variabilities and was not associated with a distortion of the CBFV step response estimates for both normocapnic and hypercapnic conditions (P=0.59 and P=0.96, respectively). Sensitivity and specificity of CA impairment detection were improved with the thigh cuff method, with the area under the receiver-operator curve increasing from 0.746 to 0.859 (P=0.031). We conclude that the new method is a safe, efficient, and appealing alternative to currently existing assessment methods for the investigation of the status of CA.

Continuous Monitoring of Cerebrovascular Reactivity Using Pulse Waveform of Intracranial Pressure

Guidelines for the management of traumatic brain injury (TBI) call for the development of accurate methods for assessment of the relationship between cerebral perfusion pressure (CPP) and cerebral autoregulation and to determine the influence of quantitative indices of pressure autoregulation on outcome. We investigated the relationship between slow fluctuations of arterial blood pressure (ABP) and intracranial pressure (ICP) pulse amplitude (an index called PAx) using a moving correlation technique to reflect the state of cerebral vasoreactivity and compared it to the index of pressure reactivity (PRx) as a moving correlation coefficient between averaged values of ABP and ICP. A retrospective analysis of prospective 327 TBI patients (admitted on neurocritical care unit of a university hospital in the period 2003-2009) with continuous ABP and ICP monitoring. PAx was worse in patients who died compared to those who survived (-0.04 ± 0.15 vs. -0.16 ± 0.15, χ2 = 28, p < 0.001). In contrast to PRx, PAx was able to differentiate between fatal and non-fatal outcome in a group of 120 patients with ICP levels below 15 mmHg (-0.04 ± 0.16 vs. -0.14 ± 0.16, χ2 = 6, p = 0.01). PAx is a new modified index of cerebrovascular reactivity which performs equally well as established PRx in long-term monitoring in severe TBI patients, but importantly is potentially more robust at lower values of ICP. In view of establishing an autoregulation-oriented CPP therapy, continuous determination of PAx is feasible but its value has to be evaluated in a prospective controlled trail.

Age-Related Impairment in Choroidal Blood Flow Compensation for Arterial Blood Pressure Fluctuation in Pigeons

Choroidal vessels compensate for changes in systemic blood pressure (BP) so that choroidal blood flow (ChBF) remains stable over a BP range of approximately 40 mm Hg above and below basal. Because of the presumed importance of ChBF regulation for maintenance of retinal health, we investigated if ChBF compensation for BP fluctuation in pigeons fails with age. Transcleral laser Doppler flowmetry was used to measure ChBF during spontaneous BP fluctuation in anesthetized pigeons ranging in age from 0.5 to 17 years (pigeons can live approximately 20 years in captivity). ChBF in <8-year-old pigeons remained near 100% of basal ChBF at BPs ranging 40 mm Hg above and below basal BP (95 mm Hg). Baroregulation failed below approximately 50 mm Hg BP. In ≥8-year-old pigeons, ChBF compensation was absent at >90 mm Hg BP, with ChBF linearly following BP. Over the 60 to 90 mm Hg range, ChBF in ≥8-year-old pigeons was maintained at 60-70% of young basal ChBF. Below approximately 55 mm Hg, baroregulation again followed BP linearly. Age-related ChBF baroregulatory impairment occurs in pigeons, with ChBF linear with above-basal BP, and ChBF failing to adequately maintain ChBF during below-basal BP. Defective autonomic sympathetic and parasympathetic neurogenic control, or defective myogenic control, may cause these baroregulatory defects. In either case, overperfusion during high BP may cause oxidative injury to the outer retina, whereas underperfusion during low BP may result in deficient nutrient supply and waste removal, with both abnormalities contributing to age-related retinal pathology and vision loss.

The Hemodynamic Effect of Total Liquid Ventilation in Piglets With Reduced Cardiac Function After Cardiopulmonary Bypass

Total liquid ventilation (TLV) is a promising treatment for severe lung injury and heart resuscitation. We aim to investigate the hemodynamic effect of TLV in piglets with preexisting cardiac dysfunction. After onset of cardiopulmonary dysfunction induced by cardiopulmonary bypass (CPB), piglets were randomly treated with TLV (n = 6) or conventional gas ventilation (n = 6) for 240 min. Hemodynamics was monitored before and at a 30-min interval after CPB. CPB with cardiac arrest resulted in significant decrease in cardiac index (CI) (96.19 ± 6.74 vs. 48.58 ± 3.96 mL/min/kg, P < 0.001) and increase of pulmonary vascular resistance (PVR) (1123.38 ± 198.97 vs. 8180.62 ± 1041.35 dyne·s/cm(5), P < 0.001). Compared with conventional gas ventilation, there was no further significant decrease of CI or increase of PVR during TLV throughout the experiment. No significant difference was observed on other hemodynamic variables including heart rate, mean arterial pressure, mean pulmonary arterial pressure, and central venous pressure between both groups. The fluctuation of mean arterial blood pressure was 3.95 ± 1.68 mm Hg during TLV. No evidence of fluorothorax or cardiac tamponade was observed in either group. We conclude that TLV does not further impair hemodynamics in piglets with preexisting cardiac dysfunction immediately after CPB.

Central pituitary adenylate cyclase-activating polypeptide (PACAP) and vasoactive intestinal peptide (VIP) decrease the baroreflex sensitivity in trout

Although PACAP and VIP exert diverse actions on heart and blood vessels along the vertebrate phylum, no information is currently available concerning the potential role of these peptides on the regulation of the baroreflex response, a major mechanism for blood pressure homeostasis. Consequently, the goal of this study was to examine in our experimental model, the unanesthetized rainbow trout Oncorhynchus mykiss, whether PACAP and VIP are involved in the regulation of the cardiac baroreflex sensitivity (BRS). Cross-spectral analysis techniques using a fast Fourier transform algorithm were employed to calculate the coherence, phase and gain of the transfer function between spontaneous fluctuations of systolic arterial blood pressure and R–R intervals of the electrocardiogram. The BRS was estimated as the mean of the gain of the transfer function when the coherence between the two signals was high and the phase negative. Compared with vehicle, intracerebroventricular (ICV) injections of trout PACAP-27 and trout VIP (25–100 pmol) dose-dependently reduced the cardiac BRS to the same extent with a threshold dose of 50 pmol for a significant effect. When injected intra-arterially at the same doses as for ICV injections, only the highest dose of VIP (100 pmol) significantly attenuated the BRS. These results suggest that the endogenous peptides PACAP and VIP might be implicated in the central control of cardiac baroreflex functions in trout.

Effects of ageing on cerebral haemodynamics assessed during respiratory manoeuvres

cerebral autoregulation (CA) is the ability to control cerebral blood flow during fluctuations in arterial blood pressure (ABP). It is impaired in a number of conditions including acute stroke, though studies so far have not found a decline in CA with age. CA is very sensitive to changes in pCO₂. this study investigates the effect of ageing on CA using a moving-window autoregressive moving average (MW-ARMA) to calculate CA as autoregulatory index (ARMA-ARI) during hypercapnia and hypocapnia, to ascertain whether this method would detect age-related differences in CA due to change in pCO₂. ECG was used to measure R-R interval, Finapres to measure ABP and capnography to measure end-tidal CO₂. Transcranial Doppler ultrasonography was used to measure left and right middle cerebral artery cerebral blood flow velocity (CBFV). Hypercapnia was induced by a breath-hold, hypocapnia by hyperventilation. thirty volunteers of mean age 25 ± 6 years and 30 volunteers of mean age 64 ± 4 years were recruited. CBFV was higher and change in CBFV due to respiratory manoeuvre was significantly greater in the younger group compared with the older group. However, no difference in ARMA-ARI was found between the groups. these findings suggest that CA is not affected by healthy ageing.

Pattern of respiratory-induced changes in fingertip blood volume measured by light transmission

Respiratory-induced fluctuations in heart rate and arterial blood pressure have been intensively investigated, but there is little information on the effect of respiration on peripheral blood volume. In the current study, blood volume changes in the finger, obtained by light transmission measurements, were measured during regular breathing (6 s periods) and long breathing (12 s periods). Respiratory chest-circumference changes were simultaneously measured in order to associate the pattern of tissue blood volume change with the respiratory cycle. Sixteen subjects were studied, and in fourteen finger blood vol ume increased during inspiration and decreased during expiration in the long-breathing periods. In all 14 subjects the start of blood volume decrease was significantly delayed from the start of expiration by mean ± SD 1.00 ± 0.65 s (p < 0.001, range 0 - 2.3 s). The start of blood volume increase was significantly delayed from the end of expiration by 3.45 ± 1.76 s (p < 0.005). In eight, finger blood volume started to increase more than 2 s before the start of inspiration. For the 6 s breathing period, blood volume decreased during inspiration in five examinations, and increased in seven. The increase in peripheral blood volume during inspiration could be attributed to the higher abdominal pressure during inspiration, and to the decrease in sympathetic activity during inspiration and the subsequent vasodilatation. The decrease in peripheral blood volume during inspiration is probably due to the negative thoracic pressure during inspiration and its mechanical effect on thoracic vessels.

Slow vasogenic fluctuations of intracranial pressure and cerebral near infrared spectroscopy—an observational study

Increased slow-wave activity in intracranial pressure (ICP) signifies an exhausted cerebrospinal compensatory reserve across a range of conditions. In this study, we attempted to describe synchronisation between slow waves of ICP and of near-infrared spectroscopy (NIRS) variables during controlled elevation of ICP. Nineteen patients presenting with symptomatic hydrocephalus underwent a Computerised Infusion Test. NIRS-derived indices, ICP and arterial blood pressure (ABP) were recorded simultaneously. ICP increased from 9.3 (6.0) mmHg to a 17.1 (8.9) mmHg during infusion. Slow waves in ICP were accompanied by concurrent waves in each NIRS variable (including deoxygenated haemoglobin (Hb) and oxygenated haemoglobin (HbO2)) with a mean coherence of >0.7 and no significant phase shift. In the same bandwidth (0.3-1.8 min(-1)), ABP fluctuations occurred with a coherence of 0.77 and phase lead of 40° with respect to ICP. The power of ICP slow waves increased significantly during infusion plateau with a corresponding increase in power of Hb waves. Slow fluctuations in cerebral oximetry as detected by NIRS coincide with and are implicated in the origin of ICP slow waves and increases during periods of exhausted cerebrospinal compensatory reserve. NIRS may be used as a non-invasive marker of increased ICP slow waves (and therefore reduced CSF compensatory reserve).

Precision of coherence analysis to detect cerebral autoregulation by near-infrared spectroscopy in preterm infants

Coherence between spontaneous fluctuations in arterial blood pressure (ABP) and the cerebral near-infrared spectroscopy signal can detect cerebral autoregulation. Because reliable measurement depends on signals with high signal-to-noise ratio, we hypothesized that coherence is more precisely determined when fluctuations in ABP are large rather than small. Therefore, we investigated whether adjusting for variability in ABP (variability(ABP)) improves precision. We examined the impact of variability(ABP) within the power spectrum in each measurement and between repeated measurements in preterm infants. We also examined total monitoring time required to discriminate among infants with a simulation study. We studied 22 preterm infants (GA<30) yielding 215 10-min measurements. Surprisingly, adjusting for variability(ABP) within the power spectrum did not improve the precision. However, adjusting for the variability(ABP) among repeated measurements (i.e., weighting measurements with high variability(ABP) in favor of those with low) improved the precision. The evidence of drift in individual infants was weak. Minimum monitoring time needed to discriminate among infants was 1.3-3.7 h. Coherence analysis in low frequencies (0.04-0.1 Hz) had higher precision and statistically more power than in very low frequencies (0.003-0.04 Hz). In conclusion, a reliable detection of cerebral autoregulation takes hours and the precision is improved by adjusting for variability(ABP) between repeated measurements.

Dynamic control of maximal ventricular elastance via the baroreflex and force-frequency relation in awake dogs before and after pacing-induced heart failure.

We investigated to what extent maximal ventricular elastance (E(max)) is dynamically controlled by the arterial baroreflex and force-frequency relation in conscious dogs and to what extent these mechanisms are attenuated after the induction of heart failure (HF). We mathematically analyzed spontaneous beat-to-beat hemodynamic variability. First, we estimated E(max) for each beat during a baseline period using the ventricular unstressed volume determined with the traditional multiple beat method during vena cava occlusion. We then jointly identified the transfer functions (system gain value and time delay per frequency) relating beat-to-beat fluctuations in arterial blood pressure (ABP) to E(max) (ABP-->E(max)) and beat-to-beat fluctuations in heart rate (HR) to E(max) (HR-->E(max)) to characterize the dynamic properties of the arterial baroreflex and force-frequency relation, respectively. During the control condition, the ABP-->E(max) transfer function revealed that ABP perturbations caused opposite direction E(max) changes with a gain value of -0.023 +/- 0.012 ml(-1), whereas the HR-->E(max) transfer function indicated that HR alterations caused same direction E(max) changes with a gain value of 0.013 +/- 0.005 mmHg.ml(-1).(beats/min)(-1). Both transfer functions behaved as low-pass filters. However, the ABP-->E(max) transfer function was more sluggish than the HR-->E(max) transfer function with overall time constants (indicator of full system response time to a sudden input change) of 11.2 +/- 2.8 and 1.7 +/- 0.5 s (P < 0.05), respectively. During the HF condition, the ABP-->E(max) and HR-->E(max) transfer functions were markedly depressed with gain values reduced to -0.0002 +/- 0.007 ml(-1) and -0.001 +/- 0.004 mmHg.ml(-1).(beats/min)(-1) (P < 0.1). E(max) is rapidly and significantly controlled at rest, but this modulation is virtually abolished in HF.

Resuscitation With Hydroxyethyl Starch Solution Prevents Bone Marrow Mononuclear Apoptosis in a Rat Trauma-Hemorrhagic Shock Model

: Trauma-hemorrhagic shock (T/HS) has been associated with multiorgan dysfunction, including bone marrow failure. This study examined apoptosis and morphologic alterations in bone marrow mononuclear cells (BMMNCs) with different volume therapies after T/HS. : T/HS was induced in groups of male Sprague-Dawley rats through a fracture of the left femur and continual bleeding for 30 minutes, followed by resuscitation with Ringer's lactate solution (RL), 6% hydroxyethyl starch solution (HES), or 5% albumin (ALB). Mean arterial blood pressure was monitored during the T/HS and resuscitation, and the impacts of various resuscitative fluids on apoptosis and morphology of BMMNCs at 24 hours and 48 hours after resuscitation were examined using flow cytometry, transferase-mediated dUTP nick-end labeling assay, and hematoxylin and eosin staining. : Fluctuations in mean arterial blood pressure were homogenous among the three treatment groups. The percentage of early BMMNC apoptosis increased significantly at 24 hours and 48 hours (24.65% +/- 5.41% and 29.09% +/- 2.07%, respectively; p < 0.05), and the percentage of late BMMNC apoptosis increased to 13.43% +/- 2.82% (p < 0.05) at 48 hours in the T/HS + RL group. In contrast, resuscitation with HES alone dramatically attenuated the apoptosis. Resuscitation with ALB alleviated BMMNC apoptosis, except for late apoptosis at 48 hours. A greater number of apoptotic BMMNCs as well as morphologic alterations were shown using the transferase-mediated dUTP nick-end labeling assay and hematoxylin and eosin stain in the T/HS + RL group than in the HES or ALB groups. : Intravascular volume replacement with HES showed prevention of BMMNC apoptosis at first 48 hours after T/HS compared with RL and ALB. These findings provide new insights into the intervention mechanism of HES on T/HS-related multiorgan dysfunction.

Wavelet Phase Synchronization Analysis of Cerebral Blood Flow Autoregulation

The dynamic relationship between beat-to-beat mean arterial blood pressure (ABP) fluctuations and cerebral blood flow velocity (CBFV) variations have been intensively studied. The experimentally observed low coherence in the low-frequency band has previously indicated that the assumptions of linearity and/or stationarity, the preconditions of the linear transfer function analysis, are not valid in that frequency region. Latka et al. [M. Latka, M. Turalska, M. Glaubic-Latka, W. Kolodziej, D. Latka, and B. J. J. West, "Phase dynamics in cerebral autoregulation," Amer. J. Physiol. Heart Circ. Physiol., vol. 289 pp. H2272-H2279, Jul. 2005] used a wavelet phase synchronization method to identify the instantaneous phase difference between ABP and CBFV, and low values of synchronization index were found in the low-frequency range, seeming to provide further evidence that the cerebral autoregulation system is nonstationary. Here, we focus on another possible factor corresponding for this low synchronization index-unmeasured variability. We demonstrate analytically and with a physiologically based cerebral hemodynamic model that, in the case of multiple inputs, the phase difference between one input, ABP, and the output, CBFV, will be distorted by an additional input, end-tidal CO(2) (P(ETCO(2))), and no longer accurately represent the true ABP-CBFV system phase shift. We also prove that this phase distortion can be corrected if the transfer functions for ABP-CBFV and P(ETCO(2))-CBFV are known or can be estimated. A significantly increased value of synchronization index in the low-frequency band is found by using the CO(2) correction term with experimental data on 13 subjects. This essentially indicates that the lack of synchronization between ABP and CBFV previously identified by Latka et al. [M. Latka, M. Turalska, M. Glaubic-Latka, W. Kolodziej, D. Latka, and B. J. J. West, "Phase dynamics in cerebral autoregulation," Amer. J. Physiol. Heart Circ. Physiol., vol. 289, pp. H2272-H2279, Jul. 2005] can be partly attributed to unmeasured variability.

Effects of heat stress on dynamic cerebral autoregulation during large fluctuations in arterial blood pressure

Impaired cerebral autoregulation during marked reductions in arterial blood pressure may contribute to heat stress-induced orthostatic intolerance. This study tested the hypothesis that passive heat stress attenuates dynamic cerebral autoregulation during pronounced swings in arterial blood pressure. Mean arterial blood pressure (MAP) and middle cerebral artery blood velocity were continuously recorded for approximately 6 min during normothermia and heat stress (core body temperature = 36.9 +/- 0.1 degrees C and 38.0 +/- 0.1 degrees C, respectively, P < 0.001) in nine healthy individuals. Swings in MAP were induced by 70-mmHg oscillatory lower body negative pressure (OLBNP) during normothermia and at a sufficient lower body negative pressure to cause similar swings in MAP during heat stress. OLBNP was applied at a very low frequency ( approximately 0.03 Hz, i.e., 15 s on-15 s off) and a low frequency ( approximately 0.1 Hz, i.e., 5 s on-5 s off). For each thermal condition, transfer gain, phase, and coherence function were calculated at both frequencies of OLBNP. During very low-frequency OLBNP, transfer function gain was reduced by heat stress (0.55 +/- 0.20 and 0.31 +/- 0.07 cm x s(-1) x mmHg(-1) during normothermia and heat stress, respectively, P = 0.02), which is reflective of improved cerebrovascular autoregulation. During low-frequency OLBNP, transfer function gain was similar between thermal conditions (1.19 +/- 0.53 and 1.01 +/- 0.20 cm x s(-1) x mmHg(-1) during normothermia and heat stress, respectively, P = 0.32). Estimates of phase and coherence were similar between thermal conditions at both frequencies of OLBNP. Contrary to our hypothesis, dynamic cerebral autoregulation during large swings in arterial blood pressure during very low-frequency (i.e., 0.03 Hz) OLBNP is improved during heat stress, but it is unchanged during low-frequency (i.e., 0.1 Hz) OLBNP.

Effects of Autoregulation and CO2 Reactivity on Cerebral Oxygen Transport

Both autoregulation and CO(2) reactivity are known to have significant effects on cerebral blood flow and thus on the transport of oxygen through the vasculature. In this paper, a previous model of the autoregulation of blood flow in the cerebral vasculature is expanded to include the dynamic behavior of oxygen transport through binding with hemoglobin. The model is used to predict the transfer functions for both oxyhemoglobin and deoxyhemoglobin in response to fluctuations in arterial blood pressure and arterial CO(2) concentration. It is shown that only six additional nondimensional groups are required in addition to the five that were previously found to characterize the cerebral blood flow response. A resonant frequency in the pressure-oxyhemoglobin transfer function is found to occur in the region of 0.1 Hz, which is a frequency of considerable physiological interest. The model predictions are compared with results from the published literature of phase angle at this frequency, showing that the effects of changes in breathing rate can significantly alter the inferred phase dynamics between blood pressure and hemoglobin. The question of whether dynamic cerebral autoregulation is affected under conditions of stenosis or stroke is then examined.

Cerebrovascular reactivity and cerebral autoregulation in normal subjects

Background Cerebrovascular reactivity (CVR) testing with CO2 challenge is used clinically as a measure of cerebrovascular reserve. However it is not known whether CVR measures the same physiological process as spontaneous cerebral autoregulation (CA). Purpose To compare CVR with CA in healthy volunteers, using continuous monitoring of cerebral blood flow velocity (CBFV) and arterial blood pressure (ABP). Methods We prospectively studied CVR and CA in 18 healthy volunteers. CVR was assessed using mean CBFV changes after 5% CO2 inhalation. CA was determined by transfer function analysis to derive the phase shift between spontaneous ABP and CBFV fluctuations at 0.1 Hz. Results CO2 inhalation produced a significant decrease in phase shift from 37.9 ± 13.8° to 21.0 ± 7.2° ( p < 0.001). In addition, there was a significant correlation between CVR and CA changes during CO2 inhalation ( R = − 0.50, p = 0.03), but not between CVR and baseline CA ( R = 0.22, p = 0.4). Conclusion We showed a decrease in spontaneous CA after vasodilatation. However, the lack of correlation between baseline CA and degree of CVR suggests that cerebrovascular reserve and CA are based in part on distinct physiological mechanisms. Further studies are needed to determine which of these parameters is most useful to guide treatment decisions in pathological states.