Theoretical model for investigating the magnetic and electric fields produced during pulsed magnetic field therapy for nonunion of the tibia

Pulsed magnetic field therapy for tibial nonunion has become an established orthopaedic procedure in many centres. The field is generated by passing pulses of current through coils positioned one each side of the limb but the magnitudes of the magnetic and induced electric fields produced are not usually known. The paper describes a method of calculating the fields that gives good agreement between theory and measurement. An improved model of a bone in a limb has been developed and this model predicts that the peak induced electric field close to the fracture site is between 0·03 and 0·6 Vm⁻¹, depending on which of the many clinically tested coil systems is used. The effect of changing geometry and the contribution of the outer surface of the limb are examined, and the implications for future experimental work are discussed.     

Electrical stimulation of cardiac myocytes

The influence of nonuniform cell shape and field orientation on the field stimulation thresholds of cardiac myocytes was studied both experimentally and computationally. The percent change in excitation threshold, which was studied with patch clamp technique, was found to be 182±83.1% (mean ±SD) higher when the electric field (EF) was parallel to the transverse cell axisversus the longitudinal axis (p<0.0006). On reversing the polarity of the applied EF, the percentage change in threshold was observed to increase by 98.9±71.0% (p<0.0002), implying asymmetry of the stimulation threshold of isolated myocytes. Finite element models were made to investigate the distribution of the transmembrane potential of these experimentally studied myocytes. A typical cell model showed that the maximum transmembrane potential induced on opposite ends of the cell was 39.1 mV and −46.5 mV for longitudinal field (aligned with the long axis of the cell), but was 40.5 mV and −44.8 mV for transverse field (aligned with the short axis of the cell). More significantly, it was found that the maximum transmembrane potential occurred at discrete points or “hot spots” on the cell membrane. It is hypothesized that the depolarization of the cell initiates at the hot spot and then spreads over the entire cell. The different excitation thresholds for different polarities of the applied EF can be explained by the different maximum induced at the opposite ends of the cell.     

Optimization of pulse train duration for the electrical stimulation of a skeletal muscle ventricle in the dog

The optimal means of electrically stimulating a skeletal muscle to contract around a fluid-filled pouch (i.e., a skeletal muscle ventricle [SMV]) has not been determined. A SMV was made from the latissimus dorsi muscle in five dogs and the rectus abdominis muscle in five dogs, and each SMV was electrically stimulated via the motor nerve(s) to contract around a fluid-filled pouch, which was connected to a mock circulatory system. The pulse train duration (PTD) was varied from 100 ms to 800 ms in 100 ms increments to determine the effect of this variable upon SMV output. The pulse width of the electrical stimulus was kept constant at 100 μs and the pulse frequency was maintained at 50s⁻¹. For SMV contraction rates of 20, 30, and 40 min⁻¹, the optimal PTD was 400 ms for both muscles. The peak output was 710 ml min⁻¹ for the rectus SMV and 556 ml min⁻¹ for the latissimus SMV. For an SMV contraction rate of 10min⁻¹, the optimal PTD was 800 ms for the rectus SMV and 600 ms for the latissimus SMV. Use of less than an optimal PTD caused reductions in SMV output of 25–50%. Although SMVs made from rectus abdominis and latissimus dorsi had similar values for the optimal PTD, the maximum SMV output was usually greater with the rectus abdominis in this acute study with untrained muscles. We conclude that PTD is an important variable to control, which can markedly affect results when studying the potential use of skeletal muscle power for cardiac assistance.     

Electrical phosphenes: on the influence of conductivity inhomogeneities and small-scale structures of the orbita on the current density threshold of excitation

Electrical and magnetic phosphenes, perceptions of light as a result of non-adequate stimulation of the eye by electrical current or magnetic induction, respectively, are one of the cornerstones to justify limit values for extreme low-frequency fields specified by statutory regulations. However, the mechanism and place of action, as well as the excitation threshold, remain unknown until now. We suggest that the origin of phosphene excitation is the synaptic layer of the eye. The current density threshold value for electrical phosphene excitation was numerically quantified for this area on the basis of a detailed geometrical model in original submillimetre resolution and specifically measured conductivities in the LF range. The threshold values found were 1.8 Am⁻² at 60 Hz and 0.3 Am⁻² at 25 Hz. These values are comparable with values of other excitable tissues. It has been shown that the current density threshold for phosphene generation depends on small-scale structures not taken into account by previous models.     

Transventricular defibrillation thresholds using quarter and half sinusoidal pulses

Transventricular peak current defibrillation thresholds using quarter (5 ms) and half (10 ms) sinusoidal pulses were determined in dogs under conditions of normothermia. For 5 ms, the overall average was 59·6 mAg⁻¹ of heart (s.d. 21·00) in a total of ten animals and 88 successful defibrillations. For 10 ms, the average over seven dogs and 51 determinations was 52·5 mAg⁻¹ of heart (s.d. 15·4). This difference was not statistically significant, whereas the energy delivered in the latter was about twice as much as in the former, suggesting the quarter sine wave pulse was better for defibrillation. A tighter definition of threshold is also introduced, i.e. the midrange between the maximum value which did not defibrillate and the minimum that did defibrillate. Such a definition is more realistic because it takes into account the successful and also the unsuccessfulvalues within a band of overlapping data points. The thresholds so obtained (52·3 mAg⁻¹, s.d. 15·7, nine dogs, 5 ms; 42·9 mAg⁻¹, s.d. 6·56, fourdogs, 10 ms) were, as expected, somewhat lower than the above mentioned ones showing, at the same time, lower coefficients of variation.     

The effect of kinin and prostaglandin inhibitors on the renal response to angiotensin-converting enzyme inhibition: a micropuncture study in the dog

It has been suggested that angiotensin-converting enzyme (ACE) inhibition is accompanied by enhanced bradykinin and prostaglandin activities, which may contribute to the renal haemodynamic actions of ACE inhibitors. Therefore we investigated renal function by clearance and micropuncture techniques in dogs maintained either on normal or low-salt diet before and after ACE inhibition with an i. v. bolus of 0.1 mg/kg ramiprilat followed by an infusion of 5 μg kg⁻¹ min⁻¹. Subgroups each comprising six dogs were also treated with either HOE-140, a bradykinin B₂ receptor antagonist, or the cyclooxygenase inhibitor indomethacin. In general, renal effects of ramiprilat were more pronounced in dogs fed on low salt than in those on normal diet. In dogs on low salt, the mean arterial pressure decreased by 20% 20 min after ramiprilat application, whereas the total renal blood flow rose by 71% from 4.71 to 8.06 ml min⁻¹ g kidney weight⁻¹ and the glomerular filtration rate (GFR) by 28% from 0.74 to 0.95 ml min⁻¹ g⁻¹. Single-nephron glomerular blood flow and single-nephron GFR rose by 55% and 23% respectively. The total and the single-nephron filtration fraction decreased by 25% and 23% respectively. There were no substantial changes in glomerular and peritubular capillary and tubular pressures, but a significant increase in the ultrafiltration coefficient, K _f, by 103% from 3.55 nl/ mmHg to 7.19 nl/mmHg (26.7–54.0 nl/kPa) was observed. Afferent and efferent arteriolar resistances decreased in parallel by 55% and 47%. Prior and concomitant intrarenal arterial infusion of HOE-140 at a dose that blocked the vasodilatory effect of 9 ng kg⁻¹ min⁻¹ bradykinin had no significant effects in dogs on low salt but attenuated the relative rise in renal and single-nephron glomerular blood flow and K _f by 21%, 27% and 26% respectively in dogs on low salt (P<0.01). No such effects were observed with indomethacin. We conclude that ACE inhibition in the dog results in a parallel decrease in afferent and efferent resistance and significantly increases K _f. This latter effect is partly mediated by the kinin system under conditions of Na⁺ depletion.     

Joule heating during solid tissue electroporation

The application of high-voltage pulses to biological tissue causes not only electroporation, a non-thermal phenomenon of pore creation within a lipid membrane due to an elevated electric field, but also significant heating. Once a biological membrane is porated, the current density increases several times, causing Joule heating. A combined experimental and theoretical study is reported. The theoretical temperature rise for a 1.25kV cm⁻¹, 6ms pulse is about 11.2K for a tissue conductivity of 0.5Sm⁻¹ (i.e. myocardial tissue) during high-voltage application. Owing to the inhomogeneous electric field obtained with the use of needle electrodes, the temperature rises first at the electrodes, where the field strength reaches a maximum. Only for highly conductive tissue such as muscle was a temperature effect primarily observed in the bulk. Even if the temperature effect is biologically insignificant, it can affect the creation of stabile aqueous pathways by electroporation. The calculation of temperature distribution during high-voltage application, taking the electric field strength and the heat transfer into account, can be a useful tool for electrode optimisation.     

Analysis of the O-wave in acute right ventricular apex impedance measurements with a standard pacing lead in animals

Modern pacemakers (implantable devices used for maintaining an appropriate heart rate in patients) can use an intracardiac ventricular impedance signal for physiological cardiac stimulation control. Intracardiac ventricular impedance from nine animal subjects is analysed and presented (seven sheep: 49.0±6.5 kg, sinus rhythm 100.3±16.5 beats min⁻¹, average impedance 629.8±72.6Ω; and two dogs: 30 kg each, sinus rhythm 86.0 beats min⁻¹, 862.1Ω and 134.0 beats min⁻¹, 1114.6Ω, respectively). The averaged curve and standard deviation curve of the impedance in sinus rhythm were analysed in MATLAB to clarify and study consistent impedance shape over one heart cycle. In eight of nine (89%) animal subjects, a consistent impedance slope change (notch) was observed in the early stage of the cardiac filling phase. This result was reproduced in an additional subject with simultaneous echocardiographical measurements of mitral valve blood flow. The notch occured soon after rapid early filling (E-wave in mitral flow) but prior to ventricular filling caused by atrial contraction, indicating that the impedance notch was caused by rapid ventricular filling and that it might be a sensed feature of diagnostic value. The intracardiac impedance notch in the present study had similar features to the non-invasive transthoracic impedance O-wave reported by others, and it is shown here that an O-wave is found in intracardiac impedance signals, strongly suggesting that the non-invasive O-wave is caused by cardiac events.     

Adrenaline diminishes K+ contractures and Ba2+-current in chicken slow skeletal muscle fibres

The effects of adrenaline and the β-adrenergic agonist isoprenaline on K⁺-evoked tension (K⁺-contracture) and Ba²⁺ current were investigated in chicken slow (anterior latissimus dorsi (ald)) muscle using isometric-tension measurements and current recording. Addition of adrenaline (10⁻⁷–10⁻⁵M) or isoprenaline (10⁻⁶–10⁻⁵ M) to the bath reduced the amplitude of the K⁺-contractures. These effects were blocked by the β-antagonist propranolol (5 × 10⁻⁶ M). External application of a cAMP analogue (8-bromo cyclic AMP; 1 × 10⁻⁴ M) also decreased the amplitude of the K⁺-contractures. To analyze the possible relationship between the induced tension reduction and effects on sarcolemmal Ca²⁺ channels, a slow action potential and a slow inward membrane current were studied in intact ald chicken muscle fibres. When the ald muscle was immersed in a Na⁺- and Cl⁻-free solution containing Ba²⁺ and depolarizing pulses were delivered from a −80 mV holding potential, the muscle fibres exhibited a small, slow Ba²⁺-dependent potential (observed at about −26 mV, peak amplitude, around −10 mV). The response was blocked by the addition of Co²⁺ (5 mM) or Cd²⁺ (2 mM). Using the three-microelectrode voltage-clamp technique, a slow inward membrane current underlying the Ba²⁺ potential could be discerned. The current had a mean threshold of −60 mV, reached maximum at about −5 mV and ranged from ca. 9 to 19 μA/cm² (depending on the external Ba²⁺ concentration). It had a mean reversal potential of +45 mV. The Ba²⁺ inward current was diminished when adrenaline or isoprenaline was added to the bath (1 × 10⁻⁵ M); however, this decrease did not occur when propranolol was present (5 × 10⁻⁶ M). These results suggest that the decreases in the tension of K⁺-contractures induced by adrenaline and isoprenaline may occur through β-adrenergic effects on sarcolemmal Ca²⁺ channels in ald chicken slow muscle fibres. This revised version was published online in July 2006 with corrections to the Cover Date.     

Effect of luminance level on electro-encephalogram alpha-wave synchronisation

A control system for the remote activation of electronic devices, based on alpha-wave synchronisation, must be robust over a wide range of lighting conditions. This study investigates the effect that low light levels have on the increase in amplitude of the occipital alpha-wave component of the human electro-encephalogram spectrum in response to eye closure. Measurements of the time required for the amplitude of the occipital alpha wave to increase above a predetermined threshold, upon eye closure, were taken from 21 subjects and at four illuminances, ranging from 2×10⁻¹ lx to 2×10⁻⁵ lx. The light source used to provide these illuminances was a featureless, uniformly illuminated white paper that subtended 30° of the visual field. Statistical analysis showed that the time to exceed threshold (TTET) upon eye closure was not independent (p<0.001) of illuminance, and that the main source of this lack of independence occurred at the lowest illuminance, 2×10⁻⁵ lx. At this luminance, the median TTET value was 15.0 s. However, at 2×10⁻⁴ lx, the median value of the TTET was 4.2 s. This is a sufficiently short time for device activation, and therefore a control system based on alpha-wave synchronisation is functional at very low light levels.     

Computationally Managed Bradycardia Improved Cardiac Energetics While Restoring Normal Hemodynamics in Heart Failure

In acute heart failure, systemic arterial pressure (AP), cardiac output (CO), and left atrial pressure (P _LA) have to be controlled within acceptable ranges. Under this condition, cardiac energetic efficiency should also be improved. Theoretically, if heart rate (HR) is reduced while AP, CO, and P _LA are maintained by preserving the functional slope of left ventricular (LV) Starling’s curve (S _L) with precisely increased LV end-systolic elastance (E _es), it is possible to improve cardiac energetic efficiency and reduce LV oxygen consumption per minute (MVO ₂). We investigated whether this hemodynamics can be accomplished in acute heart failure using an automated hemodynamic regulator that we developed previously. In seven anesthetized dogs with acute heart failure (CO < 70 mL min⁻¹ kg⁻¹, P _LA > 15 mmHg), the regulator simultaneously controlled S _L with dobutamine, systemic vascular resistance with nitroprusside and stressed blood volume with dextran or furosemide, thereby controlling AP, CO, and P _LA. Normal hemodynamics were restored and maintained (CO; 88 ± 3 mL min⁻¹ kg⁻¹, P _LA; 10.9 ± 0.4 mmHg), even when zatebradine significantly reduced HR (−27 ± 3%). Following HR reduction, E _es increased (+34 ± 14%), LV mechanical efficiency (stroke work/oxygen consumption) increased (+22 ± 6%), and MVO ₂ decreased (−17 ± 4%) significantly. In conclusion, in a canine acute heart failure model, computationally managed bradycardia improved cardiac energetic efficiency while restoring normal hemodynamic conditions.     

Modulation of the transient outward K+ current by inhibition of endothelin-A receptors in normal and hypertrophied rat hearts

Inhibition of endothelin-A (ET_A) receptors has been shown to reduce ventricular electrical abnormalities associated with cardiac failure. In this study, we investigate the effect of ET_A-receptor inhibition on the development of regional alterations of the transient outward K⁺ current (I _to) in the setting of pressure-induced left ventricular (LV) hypertrophy. Cardiac hypertrophy was induced in female Sprague–Dawley rats by stenosis of the ascending aorta (AS) for 7 days. Treatment with the selective ET_A-receptor antagonist darusentan (LU135252, 35 mg [kg body weight]⁻¹ day⁻¹) was started 1 day before the surgery. AS induced a 46% increase in the relative LV weight (p < 0.001) and caused a significant reduction in I _to (at +40 mV) in epicardial myocytes (19.5 ± 1.2 pA pF⁻¹, n = 32 vs 23.2 ± 1.2 pA pF⁻¹, n = 35, p < 0.05). Darusentan further reduced I _to in AS (15.4 ± 1.3 pA pF⁻¹, n = 37, p < 0.05) and sham-operated animals (19.8 ± 1.6 pA pF⁻¹, n = 48, ns.). The effects of AS and darusentan on I _to were significant and independent as tested by two-way analysis of variance. I _to was not affected in endocardial myocytes. These results indicate that endothelin-1 may exert a tonic effect on the magnitude of I _to in the epicardial region of the left ventricle but that ET_A-receptor activation is not necessary for the development of electrical alterations associated with pressure-induced hypertrophy.     

Sensing magnetic flux density of artificial neurons with a MEMS device

We describe a simple procedure to characterize a magnetic field sensor based on microelectromechanical systems (MEMS) technology, which exploits the Lorentz force principle. This sensor is designed to detect, in future applications, the spiking activity of neurons or muscle cells. This procedure is based on the well-known capability that a magnetic MEMS device can be used to sense a small magnetic flux density. In this work, an electronic neuron (FitzHugh–Nagumo) is used to generate controlled spike-like magnetic fields. We show that the magnetic flux density generated by the hardware of this neuron can be detected with a new MEMS magnetic field sensor. This microdevice has a compact resonant structure (700 × 600 × 5 μm) integrated by an array of silicon beams and p-type piezoresistive sensing elements, which need an easy fabrication process. The proposed microsensor has a resolution of 80 nT, a sensitivity of 1.2 V⋅T⁻¹, a resonant frequency of 13.87 kHz, low power consumption (2.05 mW), quality factor of 93 at atmospheric pressure, and requires a simple signal processing circuit. The importance of our study is twofold. First, because the artificial neuron can generate well-controlled magnetic flux density, we suggest it could be used to analyze the resolution and performance of different magnetic field sensors intended for neurobiological applications. Second, the introduced MEMS magnetic field sensor may be used as a prototype to develop new high-resolution biomedical microdevices to sense magnetic fields from cardiac tissue, nerves, spinal cord, or the brain.     

10 kHz microsecond pulsed X-ray generator utilising a hot-cathode triode with variable durations for biomedical radiography

A 10 kHz pulsed X-ray generator utilising a hot-cathode triode in conjunction with a new type of grid control device for controlling X-ray duration is described. The energy-storage condenser was charged up to 70 kV by a power supply, and the electric charges in the condenser were discharged to the X-ray tube repetitively by the grid control device. The maximum values of the grid voltage (negative value), the tube voltage, and the tube current were −1.5 kV, 70 kV, and 0.4 A, respectively. The duration of the flash X-ray pulse was primarily determined by the time constant of the grid control device and the cut-off voltage of thermoelectrons. The X-ray duration was controlled within a region of less than 1 ms; the X-ray intensity with a pulse width of 0.27 ms, a charged voltage of 70 kV, and a peak tube current of 0.4 A was 0.92 μC kg⁻¹ at 0.5 m per pulse. The maximum repetition rate was about 10 kHz, and the size of the focal spot was about 3.5×3.5 mm.     

Application of bioreactance for cardiac output assessment during exercise in healthy individuals

In patients with cardiac failure, bioreactance-based cardiac output (CO) monitoring provides a valid non-invasive method for assessing cardiac performance during exercise. The purpose of this study was to evaluate the efficacy of this technique during strenuous exercise in healthy, trained individuals. Fourteen recreational cyclists, mean (SD) age of 34 (8) years and relative peak oxygen uptake of (VO₂) 56 (6) ml kg⁻¹ min⁻¹, underwent incremental maximal exercise testing, whilst CO was recorded continuously using a novel bioreactance-based device (CO_bio). The CO_bio was evaluated against relationship with VO₂, theoretical calculation of arterial-venous oxygen difference (C(a − v) O₂) and level of agreement with an inert gas rebreathing method (CO_rb) using a Bland–Altman plot. Bioreactance-based CO measurement was practical and straightforward in application, although there was intermittent loss of electrocardiograph signal at high-intensity exercise. At rest and during exercise, CO_bio was strongly correlated with VO₂ (r = 0.84; P < 0.001), however, there was evidence of systematic bias with CO_bio providing lower values than CO_rb; mean bias (limits of agreement) −19% (14.6 to −53%). Likewise, calculated (C(a − v) O₂) was greater when determined using CO_bio than CO_rb (P < 0.001), although both devices provided values in excess of those reported in invasive studies. Bioreactance-based determination of CO provides a pragmatic approach to the continuous assessment of cardiac performance during strenuous exercise in trained individuals. Our findings, however, suggest that further work is needed to refine the key measurement determinants of CO using this device to improve measurement accuracy in this setting.     

Regulation of therapeutic and toxic effects of cardiac glycosides by electromagnetic radiations,alternating magnetic and electric fields

A model of bioassay of the toxic and therapeutic effects of cardiac glycosides (strophanthin K) was used in experiments within situ isolated hearts of laboratory frogs. This model helped reveal effective parameters of modulating the effects of electromagnetic radiations and of alternating magnetic and electric fields. Translated fromByulleten' Eksperimental'noi Biologii i Meditsiny, Vol. 118, N ^o 11, pp. 502–504, November, 1994 Presented by S. N. Golikov, Member of the Russian Academy of Medical Sciences     

The impact of exercise intensity on the release of cardiac biomarkers in marathon runners

We sought to determine the influence of exercise intensity on the release of cardiac troponin I (cTnI) and N-terminal pro-brain natriuretic peptide (NT-proBNP) in amateur marathon runners. Fourteen runners completed three exercise trials of the same duration but at exercise intensities corresponding to: (a) a competitive marathon [mean ± SD: heart rate 159 ± 7 beat min⁻¹, finish time 202 ± 14 min]; (b) 95% of individual anaerobic threshold [heart rate 144 ± 6 beat min⁻¹] and; (c) 85% of individual anaerobic threshold [heart rate 129 ± 5 beat min⁻¹]. cTnI and NT-proBNP were assayed from blood samples collected before, 30 min and 3 h post-exercise for each trial. cTnI and NT-proBNP were not different at baseline before each trial. After exercise at 85% of individual anaerobic threshold cTnI was not significantly elevated. Conversely, cTnI was elevated after exercise at 95% of individual anaerobic threshold (0.016 μg L⁻¹) and to an even greater extent after exercise at competition intensity (0.054 μg L⁻¹). Peak post-exercise values of NT-proBNP were elevated to a similar extent after all exercise trials (P < 0.05). The upper reference limit for cTnI (0.04 μg L⁻¹) was exceeded in six subjects at competition intensity. No data for NT-proBNP surpassed its upper reference limit. Peak post-exercise values for cTnI and NT-proBNP were correlated with their respective baseline values. These data suggest exercise intensity influences the release of cTnI, but not NT-proBNP, and that competitive marathon running intensity is required for cTnI to be elevated over its upper reference limit.     

A new impedance cardiograph device for the non-invasive evaluation of cardiac output at rest and during exercise: comparison with the “direct” Fick method

The objectives of this study were to evaluate the reliability and accuracy of a new impedance cardiograph device, the Physio Flow, at rest and during a steady-state dynamic leg exercise (work intensity ranging from 10 to 50 W) performed in the supine position. We compared cardiac output determined simultaneously by two methods, the Physio Flow (Q˙ _cPF) and the direct Fick (Q˙ _cFick) methods. Forty patients referred for right cardiac catheterisation, 14 with sleep apnoea syndrome and 26 with chronic obstructive pulmonary disease, took part in this study. The subjects' oxygen consumption values ranged from 0.14 to 1.19 l · min⁻¹. The mean difference between the two methods (Q˙ _cFick−Q˙ _cPF) was 0.04 l · min⁻¹ at rest and 0.29 l · min⁻¹ during exercise. The limits of agreement, defined as mean difference ± 2SD, were −1.34, +1.41 l · min⁻¹ at rest and −2.34, +2.92 l · min⁻¹ during exercise. The difference between the two methods exceeded 20% in only 2.5% of the cases at rest, and 9.3% of the cases during exercise. Thoracic hyperinflation did not alter Q˙ _cPF. We conclude that the Physio Flow provides a clinically acceptable and non-invasive evaluation of cardiac output under these conditions. This new impedance cardiograph device deserves further study using other populations and situations. Accepted: 3 April 2000     

Modification of ethylmethane sulfonate-induced mytagenesis with adrenaline

Experiments withCrepis capillaris dry seeds show that pretreatment with adrenaline hydrochloride and adrenaline hydrotartrate significantly reduces the number of aberrations induced by the supermutagen ethylmethane sulfonate. The effective concentration ranges for adrenaline adrenaline hydrotartrate and hydrochloride are 10⁻¹–10⁻⁷ M and 10⁻³–10⁻⁷ M, respectively. Adrenaline hydrochloride is more effective than adrenaline hydrotartrate (79.1vs. 65%, respectively). Translated fromByulleten' Eksperimental'noi Biologii i Meditsiny, Vol. 126, No. 10, pp. 427–429, October, 1998     

Towards Using Photo-Plethysmogram Amplitude to Measure Blood Pressure During Sleep

There is considerable interest in non-intrusive and reliable continuous ambulatory blood pressure measurement systems. Pulse amplitude is the peak to trough amplitude of the photo-plethysmogram signal. We compared pulse amplitude with a currently popular parameter, the pulse arrival time (PAT), for estimating continuous systolic blood pressure (SBP). Overnight sleep data from 18 young, healthy subjects (14 M 4 F, age 24 ± 5 years, BMI 23.8 ± 4.0 kg/m²) was analyzed. We found that pulse amplitude was more effective than PAT for estimating SBP during sleep. Mean coherence between pulse amplitude and SBP was significantly stronger than that for PAT [p < 0.001, 95% CI: 0.21–0.25 (finger), 0.11–0.14 (wrist)]. Correlation between pulse amplitude and SBP was significantly stronger than that for PAT [p < 0.001, 95% CI: 0.46–0.53 (finger), 0.13–0.20 (wrist)]. SBP estimation errors were significantly lower using pulse amplitude [p < 0.001, 95% CI: −1.55 to −1.29 mmHg (finger), −0.53 to −0.36 mmHg (wrist)]. We also found that while pulse amplitude was closely related to SBP, the relationship weakened during and around REM sleep (ANOVA of REM, transitional Wake-REM and transitional REM-Sleep versus other sleep states: F = 24.7, p < 0.001). These results suggest that pulse amplitude is potentially a more suitable measure than pulse arrival time for estimating continuous blood pressure.