Objective measurement of physiological signal-to-noise gain in the brainstem response to a synthetic vowel.

OBJECTIVE: This work investigates auditory speech processing in normal listeners through measurement of brainstem responses to the synthetic vowel /a/. METHODS: The vowel is presented in quiet and in continuous white noise with different signal-to-noise ratios (SNR) of +5, 0, -5, and -10 dB. RESULTS: In the presence of noise, transient response waves V and A are delayed when compared to those evoked in quiet, whereas the amplitude of wave V and the steepness of the slope between waves V and A are strongly reduced. The spectral component of the steady-state evoked response corresponding to the fundamental frequency (F0) of the vowel shows significantly greater amplitude and local SNR in the less severe noise conditions compared to the quiet condition. Such increases of the amplitude and SNR were not observed for the spectral component corresponding to the first formant of the vowel (F1). CONCLUSIONS: Results suggest that, at F0, both local noise suppression and signal enhancement contribute to the SNR gain. There is suppression of local noise near F1, but no signal enhancement. SIGNIFICANCE: The physiological SNR gain was estimated to be approximately +12 dB at both F0 and F1, as stimulus SNR was reduced from +5 to -10 dB.

Contribution of Resolved and Unresolved Harmonic Regions to Brainstem Speech-Evoked Responses in Quiet and in Background Noise.

Speech auditory brainstem responses (speech ABR) reflect activity that is phase-locked to the harmonics of the fundamental frequency (F0) up to at least the first formant (F1). Recent evidence suggests that responses at F0 in the presence of noise are more robust than responses at F1, and are also dissociated in some learning-impaired children. Peripheral auditory processing can be broadly divided into resolved and unresolved harmonic regions. This study investigates the contribution of these two regions to the speech ABR, and their susceptibility to noise. We recorded, in quiet and in background white noise, evoked responses in twelve normal hearing adults in response to three variants of a synthetic vowel: i) Allformants, which contains all first three formants, ii) F1Only, which is dominated by resolved harmonics, and iii) F2&F3Only, which is dominated by unresolved harmonics. There were no statistically significant differences in the response at F0 due to the three variants of the stimulus in quiet, nor did the noise affect this response with the Allformants and F1Only variants. On the other hand, the response at F0 with the F2&F3Only variant was significantly weaker in noise than with the two other variants (p<0.001). With the response at F1, there was no difference with the Allformants and F1Only variants in quiet, but was expectedly weaker with the F2&F3Only variant (p<0.01). The addition of noise significantly weakened the response at F1 with the F1Only variant (p<0.05), but this weakening only tended towards significance with the Allformants variant (p=0.07). The results of this study indicate that resolved and unresolved harmonics are processed in different but interacting pathways that converge in the upper brainstem. The results also support earlier work on the differential susceptibility of responses at F0 and F1 to added noise.

Continuous positive airway pressure improves nocturnal baroreflex sensitivity of patients with heart failure and obstructive sleep apnea.

OBJECTIVES: To determine the acute effects of continuous positive airway pressure (CPAP) on baroreceptor reflex sensitivity (BRS) for heart rate during sleep in congestive heart failure (CHF) patients with obstructive sleep apnea (OSA). DESIGN AND METHODS: In eight CHF patients with OSA not previously treated with CPAP, spontaneous BRS was assessed during overnight polysomnography prior to the onset of sleep, and during stage 2 non-rapid eye movement sleep (NREM) before, during and after application of CPAP. RESULTS: CPAP alleviated OSA and acutely increased the slope of BRS (median, 25%,75%) [from 3.9 (3.5, 4.8) to 6.2 (4.6, 26.2) ms/mmHg, P<0.05]. Increases in the slope of BRS persisted following withdrawal of CPAP [4.9 (4.3, 6.9) ms/mmHg, P<0.05]. CPAP also lowered heart rate (from 81.3 +/- 4.9 to 76.0 +/- 5.7 bpm, P< 0.05), an effect which persisted after its withdrawal (76.7 +/- 5.7 bpm, P < 0.05). Systolic blood pressure at the midpoint of the pressure range of BRS sequences fell while on CPAP (from 139 +/- 8 to 120 +/- 7 mmHg, P < 0.05), and remained lower following CPAP withdrawal (124 +/- 9 mmHg, P < 0.05). CONCLUSIONS: In CHF patients with OSA, CPAP increases acutely BRS during sleep, lowers heart rate and resets the operating point for BRS to a lower blood pressure. These effects of CPAP persist after its withdrawal, suggesting that nocturnal CPAP therapy may cause sustained improvement in the neural control of heart rate.

Effect of adenosine on heart rate variability in humans.

By stimulating afferent nerve endings in skeletal muscle, heart, kidney and the carotid body, adenosine infusion evokes a receptor-specific sympatho-excitatory reflex in humans that overrides its direct negative chronotropic effect. We tested the hypothesis that adenosine increases heart rate by suppressing parasympathetic and augmenting sympathetic components of heart rate variability. High-frequency (PH; 0.15-0.50 Hz) and low-frequency (PL; 0.05-0.15 Hz) components of heart rate variability total power (PT) were determined by spectral analysis. The ratios PH/PT and PL/PH respectively were used to estimate parasympathetic and sympathetic input to the sino-atrial node. Heart rate was recorded before and during a 5 min intravenous infusion of adenosine (140 micrograms.min-1.kg-1) in seven healthy men. Adenosine did not affect blood pressure, but increased heart rate by 33+/-6 beats/min, and reduced PT, PH, PL and PH/PT. In contrast, there was an increase in PL/PH. In a second experiment in nine men, brachial artery infusion of adenosine (15 micrograms.min-1.100 ml-1 forearm tissue) increased heart rate by 3 beats/min, had no effect on PT, PH, PL or PH/PT, yet increased PL/PH. Intra-arterial adenosine exerts a modest effect on heart rate by modulating cardiac sympathetic indices, without affecting parasympathetic indices, of heart rate variability, whereas intravenous infusion of adenosine reduces heart rate variability and raises heart rate by decreasing parasympathetic and increasing cardiac sympathetic tone. These reflex effects may become clinically relevant during adenosine stress testing, or when endogenous adenosine is increased, such as during ischaemia, exercise or vasodepressor reactions, or in heart failure.

Entrainment of blood pressure and heart rate oscillations by periodic breathing.

Cheyne-Stokes respiration (CSR) is a form of periodic breathing associated with periodic oscillations in blood pressure (BP) and heart rate (HR), which have been attributed to hypoxia and arousals from sleep. We hypothesized that periodic alterations in ventilation alone would promote oscillations in BP and HR. Seven healthy, wakeful subjects breathed in three patterns, as follows: (1) regular breathing (RB); (2) periodic breathing with three (PB3: cycle frequency = 0.035 Hz) augmented breaths alternating with 20-s apneas; and (3) periodic breathing with five (PB5: cycle frequency = 0.030 Hz) augmented breaths alternating with 20-s apneas. SaO2 remained above 95% throughout. During periodic breathing, peaks in BP and HR occurred during the ventilatory period and troughs occurred during apnea. The magnitudes of systolic BP oscillations increased significantly from RB (14 +/- 5 mm Hg) to PB3 (20 +/- 4 mm Hg) and PB5 (25 +/- 7 mm Hg; p < 0.005). HR oscillations also increased from regular breathing (13 +/- 6.0 beats/min) to PB3 (20.2 +/- 2.3 beats/min) and PB5 (20.2 +/- 4.7 beats/ min; p < 0.01). Spectral analysis showed that during periodic breathing there were discrete peaks in the spectral power of ventilation, BP, and R-wave-to-R-wave interval at the periodic breathing cycle frequencies. We conclude that oscillations in ventilation occurring during periodic breathing can amplify and entrain oscillations in BP and HR in the absence of hypoxia or arousals from sleep.

Neural and hypotensive effects of angiotensin II receptor blockade.

Angiotensin II participates in the neural regulation of the heart and circulation at both central and peripheral sites. To explore the role of endogenous angiotensin II in blood pressure regulation, we conducted a randomized double-blind crossover trial in nine young healthy men (aged 33+/-3 [mean+/-SE] years) studied in the absence of salt restriction, comparing the effect of 1 week treatment with the angiotensin II receptor antagonist losartan (100 mg daily) against placebo with respect to the following variables, recorded during supine rest: intra-arterial blood pressure (BP), heart rate (HR), forearm vascular resistance and norepinephrine appearance rate, total body norepinephrine spillover, variability of BP and HR (spectral analysis), and baroreflex sensitivity for HR (gain of the transfer function from systolic BP to HR). Blood pressure was 119+/-7/66+/-4 mm Hg (systolic BP/diastolic BP) after 1 week of placebo and 112+/-6/61+/-3 mm Hg after 1 week of losartan (P<.05). Forearm vascular resistance tended to fall, from 42.3+/-6.9 U on placebo to 32.8+/-5.0 U with losartan treatment (P=.07). Losartan had no effect on HR (60+/-3 on placebo versus 59+/-2 beats per minute with losartan), total body norepinephrine spillover (3.0+/-0.8 versus 3.3+/-1.2 nmol/min), forearm norepinephrine appearance rate (3.8+/-1.1 versus 5.3+/-1.1 pmol/100 mL forearm tissue per minute), power in the high- or low-frequency components of the HR variability and BP variability spectra or on baroreflex sensitivity for HR. Endogenous angiotensin II contributes to the maintenance of supine BP in normal subjects, studied in the absence of sodium restriction. The fall in BP caused by losartan is accompanied by a resetting of the baroreflex regulation of HR and sympathetic outflow, but baroreflex sensitivity for heart rate is not altered. Therefore, the reduction in BP observed after short-term angiotensin type 1 receptor antagonism may be achieved through a direct effect on vascular tone rather than through a primary reduction in sympathetic outflow.

Frequency domain characteristics of muscle sympathetic nerve activity in heart failure and healthy humans.

The purpose of this study was to characterize oscillations in muscle sympathetic nerve activity (MSNA) in the frequency domain in healthy subjects and patients with congestive heart failure (CHF) and to relate these to blood pressure (BP), heart rate (HR), and breathing frequency. MSNA burst frequency was significantly greater in CHF [52 +/- 21 (n = 12) vs. 35 +/- 11 (n = 19) bursts/min, P < 0.05], whereas breathing frequency and HR were similar. There was no significant difference between CHF and healthy subjects in total power, harmonic power, and nonharmonic power in the MSNA spectrum from 0 to 0.5 Hz, but low frequency power (LF, 0.05-0.15 Hz, P < 0.05) was reduced in heart failure patients. There was less coherence between BP and MSNA in the LF range, but similar spectral power in both groups in the very LF (VLF, 0-0.05 Hz) and high frequency (0.15-0.5 Hz) ranges. The transfer of MSNA oscillations into BP in the VLF (P < 0.05) and LF (P < 0.02) ranges was significantly lower in CHF, but gains in the transfer function and in the coherence between BP and MSNA and in the coherence between respiration and MSNA were similar in the two groups. These observations indicate that modulation of MSNA by the arterial baroreflex and respiration is preserved in CHF. The loss of LF power in the MSNA signal may be due to impaired neuroeffector transduction. The higher sympathetic nerve firing rate in CHF would therefore appear to be caused by factors other than the loss of regulation by these two inhibitory influences.

Sympathetic alternans. Evidence for arterial baroreflex control of muscle sympathetic nerve activity in congestive heart failure.

Alternation in the amplitude of muscle sympathetic nerve activity (MSNA) was documented in three patients with severe heart failure. In the index patient with pulsus alternans, the amplitude of MSNA was inversely related to changes in the preceding diastolic pressure with a lag time of 1.2 to 1.3 seconds, indicating that oscillations in burst amplitude are determined primarily by changes in this component of blood pressure. Spectral analysis of the blood pressure and MSNA signals identified two spectral peaks, one at the cardiac frequency and a second peak, with greater spectral power, at the alternans frequency (ie, at half the heart rate). The latter peak for both blood pressure and MSNA disappeared when alternans was abolished by nitroglycerin. The presence of sympathetic alternans in synchrony with pulsus alternans and the rapid transduction of changes in the diastolic blood pressure afferent signal to the amplitude of sympathetic outflow indicate that the arterial baroreflex control of MSNA must be active and rapidly responsive in human heart failure.

Binaural hearing in the presence of a low frequency magnetic field.

We propose the binaural auditory system as a candidate neural system that may be disrupted by exposure to relatively weak LF magnetic fields. Extracellular currents, induced by time-varying magnetic fields, may change the timing of action potentials in the auditory nerve, thereby disrupting sound localization when interaural time differences are very small. Three subjects were exposed to a 1000 Hz magnetic field--with a maximum rate of change of 2.3 T/s at the location of the cochlea--while presenting two identical 1000 Hz tones randomly delayed to the left or right ear by less than 10 microseconds. The subjects were asked whether the signal was perceived to be displaced to the left or right side of midline. After a total of over 20,000 trials, conducted at different phase angles between the field signal and the tones, there was no clear evidence for a consistent change in performance when the magnetic field was present. This, however, does not rule out an effect at other combinations of magnetic and acoustic frequencies.

Ventilatory function test values of health adult Jordanians.

A sample of 144 male, and 117 female healthy adults was selected to determine the normal ventilatory functions for Jordanians. Forced vital capacity, FEV1, and FMF 25-75% were determined using a dry bellows spirometer. Linear regression curves and nomograms were constructed for predicted values. Jordanian values for FVC and FEV1 were similar to those of Caucasians living in the western hemisphere.