Arterial Blood Pressure Oscillations Research Articles

Resonant and notch behavior in intracranial pressure dynamics

The intracranial pulse pressure is often increased when neuropathology is present, particularly in cases of increased intracranial pressure (ICP) such as occurs in hydrocephalus. This pulse pressure is assumed to originate from arterial blood pressure oscillations entering the cranium; the fact that there is a coupling between the arterial blood pressure and the ICP is undisputed. In this study, the nature of this coupling and how it changes under conditions of increased ICP are investigated. In 12 normal dogs, intracarotid and parenchymal pulse pressure were measured and their coupling was characterized using amplitude and phase transfer function analysis. Mean intracranial ICP was manipulated via infusions of isotonic saline into the spinal subarachnoid space, and changes in transfer function were monitored. Under normal conditions, the ICP wave led the arterial wave, and there was a minimum in the pulse pressure amplitude near the frequency of the heart rate. Under conditions of decreased intracranial compliance, the ICP wave began to lag behind the arterial wave and increased significantly in amplitude. Most interestingly, in many animals the pulse pressure exhibited a minimum in amplitude at a mean pressure that coincided with the transition from a leading to lagging ICP wave. This transfer function behavior is characteristic of a resonant notch system. This may represent a component of the intracranial Windkessel mechanism, which protects the microvasculature from arterial pulsatility. The impairment of this resonant notch system may play a role in the altered pulse pressure in conditions such as hydrocephalus and traumatic brain swelling. New models of intracranial dynamics are needed for understanding the frequency-sensitive behavior elucidated in these studies and could open a path for development of new therapies that are geared toward addressing the pulsation dysfunction in pathological conditions, such as hydrocephalus and traumatic brain injury, affecting ICP and flow dynamics.

A Mathematical Model to Investigate Gain-Induced Oscillation in the Human Cardiovascular System

“Mayer waves” are long-period (6 to 12 seconds) oscillations in arterial blood pressure, which have been observed and studied for more than 100 years in the cardiovascular system of humans and other mammals. A mathematical model of the human cardiovascular system is presented, incorporating parameters relevant to the onset of Mayer waves. The model is analyzed using methods of Lyapunov stability and Hopf bifurcation theory. The analysis shows that increase in the gain of the baroreflex feedback loop controlling venous volume may lead to the onset of oscillations, while changes in the other parameters considered do not affect stability of the equilibrium state. The results agree with observations of Mayer waves in human subjects, both in the period of the oscillations and in the observed age-dependence of Mayer waves. This leads to a proposed explanation of their occurrence, namely that Mayer waves are a “gain-induced instability”. African Journal of Educational Studies in Mathematics and Sciences Vol. 4 2006: pp. 77-91

Dynamic autoregulation of cutaneous circulation: differential control in glabrous versus nonglabrous skin

The purpose of this project was to test the hypothesis that, independent of neural control, glabrous and nonglabrous cutaneous vasculature is capable of autoregulating blood flow. In 10 subjects, spectral and transfer function analyses of arterial pressure and skin blood flow (laser-Doppler flowmetry) from glabrous (palm) and nonglabrous (forearm) regions were performed under three conditions: baseline, ganglionic blockade via intravenous trimethaphan administration, and trimethaphan plus oscillatory lower body negative pressure (LBNP; -5 to -10 mmHg) from 0.05 to 0.07 Hz. Oscillatory LBNP was applied to regenerate mean arterial pressure variability that was abolished by ganglionic blockade. Ganglionic blockade was verified by an absence of a heart rate response to a Valsalva maneuver. Spectral power and transfer function gain between blood pressure and skin blood flow were calculated in this oscillatory frequency range (0.05-0.07 Hz). Within this frequency range, ganglionic blockade significantly decreased spectral power of blood flow in both the forearm and palm, whereas regeneration of arterial blood pressure oscillations significantly increased spectral power of forearm blood flow but not palm blood flow. During oscillatory LBNP, transfer function gain between blood pressure and skin blood flow was significantly elevated at the forearm (0.28 +/- 0.03 to 0.53 +/- 0.02 flux units/mmHg; P < 0.05) but was reduced at the palm (4.7 +/- 0.5 to 1.2 +/- 0.1 flux units/mmHg; P < 0.05). These data show that independent of neural control of blood flow, glabrous skin has the ability to buffer blood pressure oscillations and demonstrates a degree of dynamic autoregulation. Conversely, these data suggest that nonglabrous skin has diminished dynamic autoregulatory capabilities.

Resonance in a mathematical model of baroreflex control: arterial blood pressure waves accompanying postural stress

A mathematical model of the arterial baroreflex was developed and used to assess the stability of the reflex and its potential role in producing the low-frequency arterial blood pressure oscillations called Mayer waves that are commonly seen in humans and animals in response to decreased central blood volume. The model consists of an arrangement of discrete-time filters derived from published physiological studies, which is reduced to a numerical expression for the baroreflex open-loop frequency response. Model stability was assessed for two states: normal and decreased central blood volume. The state of decreased central blood volume was simulated by decreasing baroreflex parasympathetic heart rate gain and by increasing baroreflex sympathetic vaso/venomotor gains as occurs with the unloading of cardiopulmonary baroreceptors. For the normal state, the feedback system was stable by the Nyquist criterion (gain margin = 0.6), but in the hypovolemic state, the gain margin was small (0.07), and the closed-loop frequency response exhibited a sharp peak (gain of 11) at 0.07 Hz, the same frequency as that observed for arterial pressure fluctuations in a group of healthy standing subjects. These findings support the theory that stresses affecting central blood volume, including upright posture, can reduce the stability of the normally stable arterial baroreflex feedback, leading to resonance and low-frequency blood pressure waves.

245 Prediction of Cerebral Outcome at 24 Months in Preterm Infants by NIRS in The First 24 Hours After Birth

Background: The prognostic value of cerebral NIRS in preterm infants remains controversial. Impaired autoregulation of brain perfusion quantified as high coherence between oscillations of cerebral intravascular oxygenation and arterial blood pressure in sick preterm infants has been related to intracerebral haemorrhage and hypoxic ischemic encephalopathy (Tsuji 2000).Aim: To compare cerebral NIRS parameters during the first 24 hours of life in sick preterm infants with cerebral ultrasound findings and neurological outcome at 9 and 18 months. Patients: 31 preterm infants admitted to our NICU for respiratory distress. Gestational age ranged from 26 1/7 to 32 2/7 weeks (median: 27 2/7) and birth weight from 690 to 2440 g (median: 1030 g).Methods: Total haemoglobin (tHb) and oxygenaton index (OI) was measured with NIRS using a sensor placed frontoparietally at three time points: 1) within first 6 h, 2) 12 - 16 h and 3) 24–28 h. Heart rate, arterial blood pressure (MAP), arterial oxygen saturation and transcutaneous pO2 and pCO2 were recorded simultaneously. Cerebral ultrasound examination (Acuson 128XP, 7 MHz transducer) was performed at 12 to 24 hours of life, at days 3, 7, 14 and every two weeks until discharge. Psycho-motor-developmental index (Bayley, PDI), mental-developmental index (MDI) and the neurological status were assessed in all surviving infants at nine and 18 months corrected for prematurity. A late follow-up examination was done between 3 and 10 years.Results: Nine infants died within the first 10 days. Nine months after expected date of birth 10 out of 20 survivors were classified abnormal with MDI or PDI <85. (Parents of two infants refused the examination). At 18 months corrected for prematurity 3 out of 18 infants had abnormal neurological status. Coherence between OI or tHb and MAP or heart rate did not change significantly between the three session. Intact survivors had significantly higher coherence with 0.6 (IQR 0.38– 0.84) than survivors with abnormal neurological status 0.38 (IQR 0.24–0.52) and deaths 0.28 (IQR 0.24–0.52).Conclusion: In contrast to previous studies low coherencies in the first 24 hours were associated with intraventricular haemorrhage, death or abnormal neurological outcome at 18 months or later. Consistent predictive results are obtained with coherencies between MAP or HR and OI or tHb analysed at 6, 12 and 24 hours after birth.

Aging and Arterial Blood Pressure Variability during Orthostatic Challenge

Background: It has been demonstrated that a decrease in vagal cardiac function compromises arterial blood pressure (ABP) stability during orthostatic challenge. Augmentations in low-frequency (LF) ABP oscillations are indicative of this change in autonomic hemodynamic control. Aging is associated with diminished arterial baroreflex sensitivity and vagal cardiac dysfunction. However, the effect of aging on the stability of ABP during an orthostatic challenge remains to be elucidated. Objective: The purpose of this study was to investigate ABP stability with aging during central hypovolemia induced by lower-body negative pressure (LBNP). Methods: Graded LBNP up to –40 mm Hg was applied in 16 older (65 ± 3 years of age) and 16 younger (25 ± 3 years of age) healthy adults. ABP variability was analyzed by fast Fourier transform. LF spectral density (0.04–0.15 Hz) was extracted to provide an index of vasomotor responsiveness. Results: Both LF systolic blood pressure (SBP) variability and diastolic blood pressure variability were augmented with LBNP. The rate of increase in LF SBP variability was augmented significantly greater in older as compared with younger subjects (p = 0.049). In addition, LF SBP variability was inversely correlated with decreases in pulse pressure in both age groups (r = –0.84, p = 0.01). The magnitude of the decreases in SBP and pulse pressure during LBNP was significantly affected by age, with the largest changes occurring in older subjects. The altered ABP response that manifested in older individuals was associated with a significant diminution in the reflex tachycardiac response elicited by LBNP. Conclusions: Induction of central hypovolemia via graded LBNP augments LF ABP variability. This increased ABP variability is significantly greater in older individuals. Our data suggest that aging is associated with ABP instability during orthostatic challenge.

Impaired dynamic cerebral autoregulation in eclampsia

Eclampsia is frequently associated with brain edema, cerebral infarction or hemorrhage. Its underlying cerebrovascular pathophysiology is still poorly understood. We examined cerebral autoregulation by a non-invasive multimodal assessment in a 28-year-old primaparous woman with postpartal eclampsia. Transcranial Doppler sonography showed considerably increased cerebral blood flow velocity (CBFV) of all basal cerebral vessels. Magnetic resonance imaging demonstrated multifocal vasogenic brain edema. Using transfer function analysis, a severely decreased phase shift between respiratory-induced 0.1-Hz oscillations of arterial blood pressure and CBFV was observed, indicating substantial disturbance of dynamic cerebral autoregulation (DCA). In contrast, CO(2)-vasomotor reactivity of the right middle cerebral artery was only slightly reduced. We therefore assume that the cerebral arteriolar dysfunction in eclampsia leads primarily to an impairment of the autoregulatory mechanism that is followed by different degrees of arteriolar vasodilation. Because of its probably high sensitivity to hemodynamic disturbances, assessment of DCA might be of great value in early pre-eclampsia for risk prediction of cerebral arteriopathy and eclampsia.

Dynamic cerebral autoregulation and collateral flow patterns in patients with severe carotid stenosis or occlusion.

The quality of collateral blood supply in carotid disease is pivotal for the resulting hemodynamic compromise. However, the interrelation between different patterns of collateral blood flow and actual impairment of cerebral autoregulation (CAR) has not been analyzed so far. Dynamic CAR was assessed noninvasively by the phase shift between respiratory-induced 0.1-Hz oscillations of arterial blood pressure (ABP) and cerebral blood flow velocity (CBFV) in 101 patients with severe unilateral carotid stenosis (> or = 75%) or occlusion. CO(2)-vasomotor reactivity was assessed via inhalation of 7% CO(2). Spontaneously activated collaterals via primary (anterior/posterior communicating artery, type I, n = 65) and secondary (ophthalmic artery / leptomeningeal with or without primary pathways, group II, n = 24) pathways were assessed by transcranial Doppler/duplex sonography. Signs of functional stenosis in the anterior collateral pathways were subsumed under type III (n = 12). Best dynamic CAR (phase shift) on affected sides was observed for type I (n = 65), in which values did not differ significantly from contralateral sides. Reduced phase shift values were present in type II; poorest values were observed for type III. CO(2)-reactivity differed mainly between type I and the other types. A less distinct differentiation of autoregulatory impairment was found when dividing patients into groups of different degrees of stenosis. Symptomatic patients (previous TIA/stroke) were significantly less frequent in the group with type I collateral flow and had significantly lower phase shift and CO(2)-reactivity values. In conclusion, we found that dynamic CAR is substantially impaired if secondary collateral pathways are activated or if functional stenosis in the activated anterior collateral pathway is present. These hemodynamic constellations are also associated with a higher proportion of clinically symptomatic patients. Determination of dynamic CAR by transfer function analysis represents a convenient, sensitive method for detection of cerebral hemodynamic compromise in obstructive carotid disease.

Transfer function analysis for clinical evaluation of dynamic cerebral autoregulation—a comparison between spontaneous and respiratory-induced oscillations

Oscillations of arterial blood pressure (ABP) and cerebral blood flow velocity (CBFV) can be used for non-invasive assessment of cerebral autoregulation using transfer function analysis. Either spontaneous oscillations (SPO) around 0.1 Hz or respiratory induced oscillations during deep breathing (DB) at a rate of 6/min have been used so far. We investigated 168 patients with severe carotid stenosis or occlusion to evaluate transfer function analysis and compare the SPO and DB approaches. ABP was assessed non-invasively (Finapres), CBFV was measured in the middle cerebral artery using transcranial Doppler sonography. Transfer function phase (P) and gain (G) were extracted from the respective spectra in a low (0.06–0.12 Hz) and high (0.20–0.30 Hz) frequency range (LF, HF) of SPO and from the 0.1 (LF) and 0.2 (HF) Hz peaks induced by DB. For SPO, significant side-to-side differences and differences between groups of severe and critical stenosis were found for P(LF), while P(HF) did not prove to be a significant parameter. G(LF) showed significant side-to-side differences, while G(HF) additionally differed significantly between severe and critical stenosis and occlusion, respectively. For DB, significant side-to-side differences were found for P(LF, HF). Mainly G(HF) differed significantly between the affected and contralateral sides, while both HF and LF gains showed lower values in groups with a higher degree of stenosis. Correlation between G and P values was generally poor. Using Bland–Altman plots a poor inter-method agreement was found mainly for P. Correlations between SPO and DB were higher for G than for P (LF r = 0.64 versus 0.44, HF 0.69 versus 0.28). Analysing reproducibility in 16 patients, only for P(LF, HF) of DB was a highly significant correlation found (Spearman's r up to 0.78). For G(LF, HF) correlations were significant for both SPO and DB with slightly higher r coefficients for SPO. In conclusion, the present study showed that (1) transfer functions P and G represent different information for characterization of dynamic cerebral autoregulation in the frequency domain. (2) Inter-method agreement between DB and SPO is poor for P and moderate for G values. (3) P extracted from DB has a higher reproducibility. (4) The extraction of P and G from the SPO phase spectra is critical and future work on standardizing this process is needed. (5) At present, the DB protocol might be slightly advantageous as a routine diagnostic tool.

Continuous cerebral autoregulation monitoring by cross-correlation analysis.

In order to validate cross-correlation analysis between spontaneous slow oscillations of arterial blood pressure (aBP) and intracranial pressure (ICP) or flow velocity as a means to assess the status of cerebral autoregulation continuously, we compared its results with different autoregulation bedside tests. The second aim was to check the method's stability over longer time periods. aBP, ICP, and flow velocity in the middle cerebral artery (FV(MCA)) was measured continuously in 13 critically ill comatose patients. Cross-correlation analysis was performed online and offline between aBP and ICP (CC [aBP --> ICP]) and aBP/FV(MCA) (CC [aBP --> FV(MCA)]). Three different autoregulation bedside tests (cuff deflation, transient hyperemic response, orthostatic hypotension) were performed immediately before a 29-min cross-correlation test period. In addition, continuous cross-correlation autoregulation monitoring was performed over multiple hours (in order to analyze for stability and to assess the influence of other factors). Cluster analysis revealed two main clusters. Cluster 1 (indicative for disturbed autoregulation) showed a centroid at t = -0.21 +/- 3.32 sec, r = 0.43 +/- 0.18 for CC [aBP --> ICP], and t = 0 +/- 3.14 sec, r = 0.44 +/- 0.18 for CC [aBP --> FV(MCA)]. Cluster 2 (indicative for normal autoregulation) revealed a centroid at t = 4.94 +/- 3.74 sec, r =- 0.4 +/- 0.16 for CC [aBP --> ICP], and t = 3.38 +/- 4.44 sec, r = -0.38 +/- 0.18 for CC [aBP --> FV(MCA)]. Comparison between the cross-correlation test results and the bedside tests showed a sensitivity of 44-73% for CC [aBP --> FV(MCA)], whereas CC [aBP --> ICP] was more specific (60-80%). Long-term monitoring revealed stable cross-correlation tests in about 45% of the measurement time. It is concluded that cross-correlation between aBP, ICP, and FV(MCA) is a valid means to monitor the autoregulation status continuously, although further improvement of sensitivity and specificity is needed to make it reliable for clinical decision making.

Serial blood pressure measurements.

The objective of the present investigation was to study the effects of a 60-s interval of venous congestion between two noninvasive measurements of arterial blood pressure (ABP) on the fluctuation of ABP, assessed by the standard deviation of the differences between two readings. ABP was measured in 345 successive patients, at rest, four times each. For 269 participants, one pair of readings was obtained with a 60-s interval and the other pair without an interval. For 76 patients, the first pair was read at the same interval, and the second pair had venous congestion interposed and there was no waiting interval. There was no increased ABP oscillation, either when there was no interval between ABP readings, or when venous congestion was interposed compared to pairs of ABP measurements performed with a 60-s interval. There was no increase in ABP oscillations when successive ABP readings were taken without an interval or even with venous congestion interposed. Contrary to the present belief, there seems to be no loss of reliability when blood pressure recordings are taken immediately one after another, in the clinical setting.

Inconsistent link between low-frequency oscillations: R-R interval responses to augmented Mayer waves.

Low-frequency oscillations in arterial blood pressure (Mayer waves) and R-R interval are thought to be linked through the arterial baroreflex. To delve into this relationship, we applied low (10 mmHg) and moderate (30 mmHg) lower body negative pressure (LBNP) in 10-s cycles to 18 healthy young male subjects. They showed no change in average blood pressure with this oscillatory stimulus but did show a significant decrease in R-R interval (P < 0.05) during both levels of LBNP. In addition, we succeeded in augmenting low-frequency blood pressure oscillations in a graded response to oscillatory LBNP level (P < 0.05) while significantly increasing low-frequency R-R interval oscillations (P < 0.05). However, cross-spectral coherence between these increased oscillations was highly variable across individuals and stimulus level. Although nearly all subjects showed significant coherence during basal conditions (n = 17), only seven subjects maintained significant coherence during both levels of LBNP. These results suggest that a complex interaction of regulatory mechanisms determines the link between low-frequency oscillations and the responses to even low levels of LBNP.

Arterial blood pressure oscillation after active standing up in kidney transplant recipients

Dynamic arterial blood pressure (FINAPRES) response to active standing up, normally consisting of initial rise, fall and recovery above the baseline (overshoot), was compared with the early steady-state arterial blood pressure level to measure sympathetic vasomotor function in healthy subjects [group 1: n=50, 10 female subjects, age 51±2.5 years; weight 78±2.3 kg; height 174±1.4 cm (mean±standard error of the mean)] and in kidney transplant recipients under basal (group 2a: n=50, age 51.7±1.7 years; weight 77±2.1 kg; height 174±1.5 cm) and under high (group 2b: same subjects as in group 2a) ciclosporine A whole blood levels. Furthermore, baroreflex sensitivity and the activity of the generating compounds of the sympathetic nervous systems (Mayer waves) were measured. Systolic and diastolic overshoot values did not differ statistically significant in the present study. In the control subjects, a systolic overshoot of 15.4±2.7 mmHg and a diastolic overshoot of 15.2±2 mmHg was detected. The systolic overshoot disappeared in 57% of group 2a (−7.1±2.7 mmHg; P<0.001) and in 50% of group 2b recipients (−8.0±2.7 mmHg; P<0.001). Systolic early steady-state level was not lower in kidney transplant recipients before ciclosporine (baseline+2 mmHg) intake, but after ciclosporine administration (baseline−3 mmHg; controls: baseline+3 mmHg; P<0.05). There was a strong association between the overshoot and steady-state levels ( P for χ 2<0.001, n=150). Overshoot of group 1 levels ( r=0.428; P<0.01) and group 2 levels ( r=0.714; P<0.001) correlated to their respective steady-state blood pressure. Furthermore, recipients had reduced baroreceptor sensitivities estimated by sequence analysis as compared to controls (10±1 ms/mmHg vs. 7.5±1.4 ms/mmHg; P<0.05). Mayer waves amplitudes of the heart rate spectrum were elevated statistically significant in renal transplant recipients (44.4±0.2 vs. 43.8±2.2 A.U.). In conclusion, baroreceptor reflex-dependent overshoot of the arterial blood pressure after active standing up is diminished in kidney transplant recipients, whereas no association to the ciclosporine A whole blood level has been detected. The reduced overshoot may be due to the diminished baroreceptor sensitivity which could be shown in renal transplant recipients.

Spontaneous oscillations of arterial blood pressure, cerebral and peripheral blood flow in healthy and comatose subjects

Slow and rhythmic spontaneous oscillations of cerebral and peripheral blood flow occur within frequencies of 0.5-3 min~1 (0.008-0.05 Hz, B-waves) and 3-9 min~1 (0.05-0.15 Hz, M-waves). The generators and pathways of such oscillations are not fully understood. We compared the coefficient of variance (CoV), which serves as an indicator for the amplitude of oscillations and is calculated as the percent standard deviation of oscillations within a particular frequency band from the mean, to study the impairment of generators or pathways of such oscillations in normal subjects and comatose patients in a controlled fashion. With local ethic committee approval, data were collected from 19 healthy volunteers and nine comatose patients suffering from severe traumatic brain injury (n = 3), severe subarachnoid hemorrhage (n = 3), and intracerebral hemorrhage (n = 3). Cerebral blood flow velocities were measured by transcranial Doppler ultrasound (TCD), peripheral vasomotion by finger tip laser Doppler flowmetry (LDF), and ABP by either non-invasive continuous blood pressure recordings (Finapres method) in control subjects, or by direct radial artery recordings in comatose patients. Each recording session lasted ~ 20-30 min. Data were stored in the TCD device for offline analysis of CoV. For CoV in the cerebral B-wave frequency range there was no difference between coma patients and controls, however there was a highly significant reduction in the amplitude of peripheral B-wave LDF and ABP vasomotion (3.8 ±2.1 vs. 28.2 ± 76.7 for LDF, p < 0.00 7; and 1.2±0.7 vs. 4.6±2.8 for ABP, p < 0.001) This observation was confirmed for spontaneous cerebral and peripheral oscillations in the M-wave frequency range. The CoV reduction in peripheral LDF and ABP oscillations suggest a severe impairment of the proposed sympathetic pathway in comatose patients. The preservation of central TCD oscillations argues in favor of different pathways and/or generators of cerebral and peripheral B- and M-waves. [Neurol Res 1999; 21: 665-669]

Intracranial pressure B-waves precede corresponding arterial blood pressure oscillations in patients with suspected normal pressure hydrocephalus

B-waves are rhythmic oscillations of intracranial pressure (ICP) with a wavelength of 0.5-2 min. These oscillations are accompanied by corresponding fluctuations of arterial blood pressure (BP). There is controversy in the literature whether the ICP oscillations precede or follow the BP oscillations. This relationship, however, is important for the understanding of the origin and the interactions of ICP B-waves with other parameters. ICP and BP were monitored continuously for one night in nine patients with suspected symptomatic normal pressure hydrocephalus (NPH). Forty-five B-waves were identified and the time delays between the peaks and the onsets of B-waves and their BP-equivalents were measured. The mean (± standard deviation) of the time delays between the peaks of ICP B-waves and corresponding BP-oscillations was 4.2 ±2.4 sec and between the onsets of the oscillations 7 0.3 ±6.6 sec. In all but two B-waves, the ICP peak preceded the BP peak, in all the 45 B-waves the onset of the ICP increase preceded the BP increase (p < 0.004). Our study demonstrates that ICP B-waves precede concomitant changes in BP by several seconds. [Neurol Res 1999; 21: 627-630]

Power spectral analysis of short-term RR interval and arterial blood pressure oscillations in the lizard, Gallotia galloti: effects of sympathetic blockade.

The role of the sympathetic limb of the autonomic nervous system (ANS) in the mediation of oscillations in consecutive beat-to-beat RR interval (RRI) and systolic blood pressure (SBP) values of lizards, Gallotia galloti, was investigated using spectral analysis and measuring effects of autonomic blockers. alpha-Adrenergic blockade decreased the power spectral density (PSD) of both RRI and SBP very low frequency (VLF: 0.007-0.055 Hz) and low frequency (LF: 0.055-0.150 Hz) bands, whereas beta-adrenergic blockade increased the PSD of both RRI- and SBP-VLF and RRI- and SBP-LF bands. These findings suggest that in lizards 1) the VLF and LF peaks of RRI and SBP power spectra are alpha-adrenergic mediated, and that 2) the beta-adrenergic activity of the sympathetic system may act buffering all RRI and SBP oscillations below 0.150 Hz. These results, when analyzed jointly with the ones obtained from a previous study (De Vera and González. 1997. Comp Biochem Physiol 85A:389-394) on the effects of parasympathetic blockade on lizards' RRI and SBP oscillations, demonstrate that these reptiles, like mammals, exhibit spontaneous short-term oscillations in their HR and SBP which are mediated by the ANS. However, unlike mammals, the RRI and ABP low-frequency oscillations in Gallotia seem to be similarly affected by the ANS and appear to be powered by alpha-adrenergic and parasympathetic activities and buffered by beta-adrenergic activity.

Gain-induced oscillations in blood pressure.

"Mayer waves" are long-period (6 to 12 seconds) oscillations in arterial blood pressure, which have been observed and studied for more than 100 years in the cardiovascular system of humans and other mammals. A mathematical model of the human cardiovascular system is presented, incorporating parameters relevant to the onset of Mayer waves. The model is analyzed using methods of Liapunov stability and Hopf bifurcation theory. The analysis shows that increase in the gain of the baroreflex feedback loop controlling venous volume may lead to the onset of oscillations, while changes in the other parameters considered do not affect stability of the equilibrium state. The results agree with clinical observations of Mayer waves in human subjects, both in the period of the oscillations and in the observed age-dependence of Mayer waves. This leads to a proposed explanation of their occurrence, namely that Mayer waves are a gain-induced oscillation.

Spontaneous blood pressure oscillations and cerebral autoregulation.

The relationship between spontaneous oscillations in cerebral blood flow velocity (CBFV) and arterial blood pressure (ABP) was analysed in normal subjects in order to evaluate whether these relationships provide information about cerebral autoregulation. CBFV was measured using transcranial Doppler sonography and continuous ABP and heart rate using Finapres in 50 volunteers. Measurements were made over 5 min in a supine position and 6 min in a tilted position. Coefficients of variation were calculated using power- and cross-spectral analysis in order to quantify amplitudes within two frequency ranges: 3-9 cycles per min (cpm) (M-waves); and 9-20 cpm (R-waves). Correlations, coherence values, phase angle shifts and gains were also computed between corresponding waves in CBFV and in ABP. A clear correlation was seen for M-waves and R-waves between CBFV and ABP and coherence values were large enough to calculate phase angle shifts and gains. Phase angles for M-waves were larger and gains lower than was the case for R-waves, either tilted or supine. These data are consistent with a highpass filter model of cerebral autoregulation. Relatively high CBFV/ABP gain values (between 1.4 and 2.0) suggest that the principle of frequency-dependent vascular input impedances has to be considered in addition to autoregulatory feedback mechanisms. Spontaneous ABP oscillations in the M-wave and R-wave ranges may serve as a basis for continuous autoregulation monitoring.

Power spectral analysis of short-term RR interval and arterial blood pressure oscillations in lizard ( Gallotia galloti): Effects of parasympathetic blockade

Spontaneous short-term oscillations in consecutive beat-to-beat RR interval (RRI) and systolic blood pressure (SBP) values of lizards ( Gallotia galloti) in basal conditions and under parasympathetic blockade with atropine at 23°C body temperature were investigated using spectral analysis. In control conditions, both RRI and SBP spectra exhibited two major oscillations in very low (VLF 0.008–0.030 Hz) and low (LF 0.030–0.100 Hz) frequencies. Most lizards presented a high frequency (HF) respiratory peak in the SBP spectra whenever the lizard's ventilatory pattern was rhythmic. Parasympathetic blockade decreased all RRI oscillations and LF and HF oscillationsof SBP. VLF and LF oscillations of RRI and SBP were still clearly present after blockade, which shows that other neural or humoral systems different from parasympathetic could mediate also low frequency RRI and SBP variability. SBP-RRI cross-spectral analysis showed in control conditions a linear relationship between SBP and RRI variations in the VLF, LF and HF bands, with SBP variations leading RRI; the parasympathetic limb of the baroreflex seems to be involved in maintaining the SBP-RRI coherence in the LF and perhaps in the HF band.

Autonomic evaluation by means of standard tests and power spectral analysis in multiple sclerosis.

Standard autonomic tests [heart rate response to deep breathing (HRDB), change in systolic blood pressure due to tilt], and spectral analysis of heart rate (HR), arterial blood pressure (ABP), and the associated transfer function analysis (gains and phases) were performed in 20 patients with multiple sclerosis to determine their diagnostic value. Transfer function analysis suggested impairment of baroreflex function in 7 patients and an alteration of cardiorespiratory coupling on a brain stem level in 4 patients. In addition, sympathetic vasomotor outflow was reduced in 2 patients (spectral ABP measures in the mid frequency band) and a decrease of vagal outflow was suggested by abnormal respiratory HR parameters in another 2 patients. An abnormal HRDB was present in 5 patients and was probably due to a central alteration (cardiorespiratory coupling) in 2 patients and due to diminished respiratory effort in 1 patient. Spectral analysis of both HR and ABP oscillations and their transfer function may considerably improve the pathophysiological interpretation of cardiovascular autonomic dysfunction in patients with central nervous system disease.