Transpulmonary speed of sound input into the supraclavicular space.

The transpulmonary speed of sound input at the mouth has been shown to vary with lung volume. To avoid the disadvantages that exist in certain clinical situations in inputting sound at the mouth, we input sound in the supraclavicular space of 21 healthy volunteers to determine whether similar information on the relationship of sound speed to lung volume could be obtained. We measured the transit time at multiple microphones placed over the chest wall using a 16-channel lung sound analyzer (Stethographics). There was a tight distribution of transit times in this population of subjects. At functional residual capacity, it was 9 +/- 1 (SD) ms at the apical sites and 13 +/- 1 ms at the lung bases. The sound speed at total lung capacity was 24 +/- 2 m/s and was 22 +/- 2 m/s at residual volume (P < 0.001). In all subjects, the speed of sound was faster at higher lung volume. This improved method of studying the mechanism of sound transmission in the lung may help in the development of noninvasive tools for diagnosis and monitoring of lung diseases.     

Sound transmission between 50 and 600 Hz in excised pig lungs filled with air and helium.

This study measured transit time (TT) and attenuation of sound transmitted through six pairs of excised pig lungs. Single-frequency sounds (50-600 Hz) were applied to the tracheal lumen, and the transmitted signals were monitored on the tracheal and lung surface using microphones. The effect of varying intrapulmonary pressure (Pip) between 5 and 25 cmH(2)O on TT and sound attenuation was studied using both air and helium (He) to inflate the lungs. From 50 to approximately 200 Hz, TT decreased from 4.5 ms at 50 Hz to 1 ms at 200 Hz (at 25 cmH(2)O). Between approximately 200 and 600 Hz, TT was relatively constant (1.1 ms at upper and 1.5 ms at lower sites). Gas density had very little effect on TT (air-to-He ratio of approximately 1.2 at upper sites and approximately 1 at lower sites at 25 cmH(2)O). Pip had marked effects (depending on gas and site) on TT between 50 and 200 Hz but no effect at higher frequencies. Attenuation was frequency dependent between 50 and 600 Hz, varying between -10 and -35 dB with air and -2 and -28 dB with He. Pip also had strong influence on attenuation, with a maximum sensitivity of 1.14 (air) and 0.64 dB/cmH(2)O (He) at 200 Hz. At 25 cmH(2)O and 200 Hz, attenuation with air was about three times higher than with He. This suggests that sound transmission through lungs may not be dominated by parenchyma but by the airways. The linear relationship between increasing Pip and increasing attenuation, which was found to be between 50 and approximately 100 Hz, was inverted above approximately 100 Hz. We suggest that this change is due to the transition of the parenchymal model from open to closed cell. These results indicate that acoustic propagation characteristics are a function of the density of the transmission media and, hence, may be used to locate collapsed lung tissue noninvasively.     

Respiratory dynamics during laughter.

Lung and chest wall mechanics were studied during fits of laughter in 11 normal subjects. Laughing was naturally induced by showing clips of the funniest scenes from a movie by Roberto Benigni. Chest wall volume was measured by using a three-dimensional optoelectronic plethysmography and was partitioned into upper thorax, lower thorax, and abdominal compartments. Esophageal (Pes) and gastric (Pga) pressures were measured in seven subjects. All fits of laughter were characterized by a sudden occurrence of repetitive expiratory efforts at an average frequency of 4.6 +/- 1.1 Hz, which led to a final drop in functional residual capacity (FRC) by 1.55 +/- 0.40 liter (P < 0.001). All compartments similarly contributed to the decrease of lung volumes. The average duration of the fits of laughter was 3.7 +/- 2.2 s. Most of the events were associated with sudden increase in Pes well beyond the critical pressure necessary to generate maximum expiratory flow at a given lung volume. Pga increased more than Pes at the end of the expiratory efforts by an average of 27 +/- 7 cmH2O. Transdiaphragmatic pressure (Pdi) at FRC and at 10% and 20% control forced vital capacity below FRC was significantly higher than Pdi at the same absolute lung volumes during a relaxed maneuver at rest (P < 0.001). We conclude that fits of laughter consistently lead to sudden and substantial decrease in lung volume in all respiratory compartments and remarkable dynamic compression of the airways. Further mechanical stress would have applied to all the organs located in the thoracic cavity if the diaphragm had not actively prevented part of the increase in abdominal pressure from being transmitted to the chest wall cavity.     

Detection of porcine oleic acid-induced acute lung injury using pulmonary acoustics.

To evaluate the utility of monitoring the sound-filtering characteristics of the respiratory system in the assessment of acute lung injury (ALI), we injected a multifrequency broadband sound signal into the airway of five anesthetized, intubated pigs, while recording transmitted sound over the trachea and on the chest wall. Oleic acid injections effected a severe lung injury predominantly in the dependent lung regions, increasing venous admixture from 6 +/- 1 to 54 +/- 8% (P < 0.05) and reducing dynamic respiratory system compliance from 19 +/- 0 to 12 +/- 2 ml/cmH(2)O (P < 0.05). A two- to fivefold increase in sound transfer function amplitude was seen in the dependent (P < 0.05) and lateral (P < 0.05) lung regions; no change occurred in the nondependent areas. High within-subject correlations were found between the changes in dependent lung sound transmission and venous admixture (r = 0.82 +/- 0.07; range 0.74-0.90) and dynamic compliance (r = -0.87 +/- 0.05; -0.80 to -0.93). Our results indicate that the acoustic changes associated with oleic acid-induced lung injury allow monitoring of its severity and distribution.     

Early detection of pulmonary congestion and edema in dogs by using lung sounds

Five mongrel dogs (2 interstitial and 3 alveolar edema) were studied. Lung mechanics were measured by recording the flow, volume, and esophageal pressure according to the standard technique. Edema was produced by infusion of Ringer lactate solution. Lung sounds were recorded on tape from the dependent part of the chest wall. Lung sound signals were high-pass filtered at 100 Hz and subjected to fast Fourier transform. Samples of lung sounds were analyzed before (control) and at 5, 10, 20, 30, and 40 min after the infusion. The mean, median, and mode frequencies of sound power spectra at the control time were, respectively, 169.6 +/- 29.19, 129.6 +/- 29.81, and 136.0 +/- 29.87 (SD) Hz. These values increased significantly at 5 min after infusion to 194.0 +/- 26.08 (P less than 0.0037), 150.2 +/- 23.48 (P less than 0.0085), and 164.6 +/- 28.74 Hz (P less than 0.02), respectively. These values stayed significantly elevated at 10, 20, 30, and 40 min. The pulmonary wedge pressure, lung dynamic compliance, and pulmonary resistance were measured also at the same times. The mean, median, and mode frequencies correlated with pulmonary wedge pressure (P less than 0.00001, P less than 0.0001, P less than 0.0001), lung dynamic compliance (P less than 0.001, P less than 0.0001, P less than 0.0001), and pulmonary resistance (P less than 0.00001, P less than 0.00001, P less than 0.0001), respectively. There were no significant adventitious sounds up to 40 and 50 min after infusion. We concluded that pulmonary congestion and early edema alter the frequency characteristics of lung sounds early, before the occurrence of adventitious sounds. These altered lung sounds may be used as an index of pulmonary congestion and impending edema.     

Acoustic characterisation of thoracic body tissues in the audible frequency range

A previous study by Jones and Thomas [2] suggests that data relating to the physiological condition within the thoracic cavity may be obtainable utilising low frequency acoustic signals applied to the mouth and detected on the chest wall. In order to evaluate the contribution to the mouth to chest wall frequency response of the separate elements within the thorax, and to estimate the effect on this response when the lung physiology changes, an acoustic model of the thorax is required. To aid the development of this model, experiments have been carried out in order to establish the frequency dependence of the acoustic attenuation and speed of propagation through thoracic tissue samples in the audible frequency range 20–500 Hz. Samples from the porcine family were used due to their physical similarity to those of humans and their being obtainable within a short time of death.The results of this work can be utilised in the development of an acoustic model of the human thorax, this in turn enabling simulation and analysis of low frequency acoustic transmission from the trachea to the chest wall.     

Low-frequency respiratory mechanical impedance in the rat

A modified forced oscillatory technique was used to determine the respiratory mechanical impedances in anesthetized, paralyzed rats between 0.25 and 10 Hz. From the total respiratory (Zrs) and pulmonary impedance (ZL), measured with pseudorandom oscillations applied at the airway opening before and after thoracotomy, respectively, the chest wall impedance (ZW) was calculated as ZW = Zrs - ZL. The pulmonary (RL) and chest wall resistances were both markedly frequency dependent: between 0.25 and 2 Hz they contributed equally to the total resistance falling from 81.4 +/- 18.3 (SD) at 0.25 Hz to 27.1 +/- 1.7 kPa.l-1 X s at 2 Hz. The pulmonary compliance (CL) decreased mildly, from 2.78 +/- 0.44 at 0.25 Hz to 2.36 +/- 0.39 ml/kPa at 2 Hz, and then increased at higher frequencies, whereas the chest wall compliance declined monotonously from 4.19 +/- 0.88 at 0.25 Hz to 1.93 +/- 0.14 ml/kPa at 10 Hz. Although the frequency dependence of ZW can be interpreted on the basis of parallel inhomogeneities alone, the sharp fall in RL together with the relatively constant CL suggests that at low frequencies significant losses are imposed by the non-Newtonian resistive properties of the lung tissue.     

Measurement and theory of wheezing breath sounds

We measured the time and frequency domain characteristics of breath sounds in seven asthmatic and three nonasthmatic wheezing patients. The power spectra of the wheezes were evaluated for frequency, amplitude, and timing of peaks of power and for the presence of an exponential decay of power with increasing frequency. Such decay is typical of normal vesicular breath sounds. Two patients who had the most severe asthma had no exponential decay pattern in their spectra. Other asthmatic patients had exponential patterns in some of their analyzed sound segments, with a range of slopes of the log power vs. log frequency curves from 5.7 to 17.3 dB/oct (normal range, 9.8-15.7 dB/oct). The nonasthmatic wheezing patients had normal exponential patterns in most of their analyzed sound segments. All patients had sharp peaks of power in many of the spectra of their expiratory and inspiratory lung sounds. The frequency range of the spectral peaks was 80-1,600 Hz, with some presenting constant frequency peaks throughout numerous inspiratory or expiratory sound segments recorded from one or more pickup locations. We compared the spectral shape, mode of appearance, and frequency range of wheezes with specific predictions of five theories of wheeze production: 1) turbulence-induced wall resonator, 2) turbulence-induced Helmholtz resonator, 3) acoustically stimulated vortex sound (whistle), 4) vortex-induced wall resonator, and 5) fluid dynamic flutter. We conclude that the predictions by 4 and 5 match the experimental observations better than the previously suggested mechanisms. Alterations in the exponential pattern are discussed in view of the mechanisms proposed as underlying the generation and transmission of normal lung sounds. The observed changes may reflect modified sound production in the airways or alterations in their attenuation when transmitted to the chest wall through the hyperinflated lung.     

Impedance and relative displacements of relaxed chest wall up to 4 Hz

We measured the effective resistance (Reff) and elastance (Eeff) of the chest wall in four subjects, relaxed at functional residual capacity (FRC), during sinusoidal volume changes (5% vital capacity up to 4 Hz) delivered at the mouth. Subjects sat in a head-out body plethysmograph, and transthoracic pressure was measured with an esophageal balloon. Changes in Reff and in Eeff with frequency were nearly the same in all subjects. Reff (in cmH2O X l-1 X s) was 2.9 +/- 0.8 at 0.2 Hz and fell sharply to minimum values (0.5-0.9) at 1-4 Hz. Eeff (in cmH2O X l-1) increased from approximately 10 at the lowest frequency to a plateau of about 15 at 1-3 Hz and decreased above 3 Hz. In the same subjects, we measured the relative magnitude and phase between the displacements of different parts of the chest wall with magnetometers during identical sinusoidal forcing. Results indicate that the chest wall expands and deflates uniformly at frequencies up to 1 Hz. Thereafter the abdomen makes relatively larger excursions, and the relative magnitude and phase of displacement at different points on the chest wall show complex changes. We conclude that the frequency dependence of Reff and Eeff below 1 Hz is not due to nonuniformities in displacement of different parts of the chest wall. The frequency dependency of Reff is consistent with an increasing contribution of rate-independent plastic dissipation to the pressure difference in phase with flow as breathing frequency decreases.     

Sound transmission in the lung as a function of lung volume.

We were interested in how the transmission of sound through the lung was affected by varying air content in intact humans as a method of monitoring tissue properties noninvasively. To study this, we developed a method of measuring transthoracic sound transit time accurately. We introduced a "coded" sound at the mouth and measured the transit time at multiple microphones placed over the chest wall by using a 16-channel lung sound analyzer (Stethographics). We used a microphone placed over the neck near the trachea as our reference and utilized cross-correlation analysis to calculate the transit times. The use of the coded sound, composed of a mix of frequencies from 130 to 150 Hz, greatly reduced the ambiguity of the cross-correlation function. The measured transit time varied from 1 ms at the central locations to 5 ms at the lung bases. Our results also indicated that transit time at all locations decreased with increasing lung volume. We found that these results can be described in terms of a model in which sound transmission through the lung is treated as a combination of free-space propagation through the trachea and a propagation through a two-phase system in the parenchyma.     

Volume-dependent variations of regional lung sound, amplitude, and phase.

Acoustic imaging of the respiratory system demonstrates regional changes of lung sounds that correspond to pulmonary ventilation. We investigated volume-dependent variations of lung sound phase and amplitude between two closely spaced sensors in five adults. Lung sounds were recorded at the posterior right upper, right lower, and left lower lobes during targeted breathing (1.2 +/- 0.2 l/s; volume = 20-50 and 50-80% of vital capacity) and passive sound transmission (< or =0.2 l/s; volumes as above). Average sound amplitudes were obtained after band-pass filtering to 75-150, 150-300, and 300-600 Hz. Cross correlation established the phase relation of sound between sensors. Volume-dependent variations in phase (< or =1.5 ms) and amplitude (< or =11 dB) were observed at the lower lobes in the 150- to 300-Hz band. During inspiration, increasing delay and amplitude of sound at the caudal relative to the cranial sensor were also observed during passive transmission in several subjects. This previously unrecognized behavior of lung sounds over short distances might reflect spatial variations of airways and diaphragms during breathing.     

Lung and chest wall mechanics in rabbits during high-frequency body-surface oscillation

In eight anesthetized and tracheotomized rabbits, we studied the transfer impedances of the respiratory system during normocapnic ventilation by high-frequency body-surface oscillation from 3 to 15 Hz. The total respiratory impedance was partitioned into pulmonary and chest wall impedances to characterize the oscillatory mechanical properties of each component. The pulmonary and chest wall resistances were not frequency dependent in the 3- to 15-Hz range. The mean pulmonary resistance was 13.8 +/- 3.2 (SD) cmH2O.l-1.s, although the mean chest wall resistance was 8.6 +/- 2.0 cmH2O.l-1.s. The pulmonary elastance and inertance were 0.247 +/- 0.095 cmH2O/ml and 0.103 +/- 0.033 cmH2O.l-1.s2, respectively. The chest wall elastance and inertance were 0.533 +/- 0.136 cmH2O/ml and 0.041 +/- 0.063 cmH2O.l-1.s2, respectively. With a linear mechanical behavior, the transpulmonary pressure oscillations required to ventilate these tracheotomized animals were at their minimal value at 3 Hz. As the ventilatory frequency was increased beyond 6-9 Hz, both the minute ventilation necessary to maintain normocapnia and the pulmonary impedance increased. These data suggest that ventilation by body-surface oscillation is better suited for relatively moderate frequencies in rabbits with normal lungs.     

Transmission of airway pressure to pleural space during lung edema and chest wall restriction

To investigate the influence of positive end-expiratory pressure (PEEP) on hemodynamic measurements we examined the transmission of airway pressure to the pleural space during varying conditions of lung and chest wall compliance. Eight ventilated anesthetized dogs were studied in the supine position with the chest closed. Increases in pleural pressure were similar for both small and large PEEP increments (5-20 cmH2O), whether measured in the esophagus (Pes) or in the juxtacardiac space by a wafer sensor (Pj). Increments in Pj exceeded the increments in Pes at all levels of PEEP and under each condition of altered lung and chest wall compliance. When chest wall compliance was reduced by thoracic and abdominal binding, the fraction of PEEP sensed in the pleural space increased as theoretically predicted. Acute edematous lung injury produced by oleic acid (OA) did not alter the deflation limb pressure-volume characteristics of the lung, provided that end-inspiratory volume was adequate. With the chest and abdomen restricted OA was associated with less than normal transmission of airway pressure to the pleural space, most likely because the end-inspiratory volume required to restore normal deflation characteristics was not attained. Together these results indicate that the influence of acute edematous lung injury on the transmission of airway pressure to the pleural space depends importantly on the peak volume achieved during inspiration.     

Forced oscillatory impedance of the respiratory system at low frequencies

Respiratory mechanical impedances were determined during voluntary apnea in five healthy subjects, by means of 0.25- to 5-Hz pseudo/random oscillations applied at the mouth. The total respiratory impedance was partitioned into pulmonary (ZL) and chest wall components with the esophageal balloon technique; corrections were made for the upper airway shunt impedance and the compressibility of alveolar gas. Neglect of these shunt effects did not qualitatively alter the frequency dependence of impedances but led to underestimations in impedance, especially in the chest wall resistance (Rw), which decreased by 20-30% at higher frequencies. The total resistance (Rrs) was markedly frequency dependent, falling from 0.47 +/- 0.06 (SD) at 0.25 Hz to 0.17 +/- 0.01 at 1 Hz and 0.15 +/- 0.01 kPa X l-1 X s at 5 Hz. The changes in Rrs were caused by the frequency dependence of Rw almost exclusively between 0.25 and 2 Hz and in most part between 2 and 5 Hz. The effective total respiratory (Crs,e) and pulmonary compliance were computed with corrections for pulmonary inertance derived from three- and five-parameter model fittings of ZL. Crs,e decreased from the static value (1.03 +/- 0.18 l X kPa-1) to a level of approximately 0.35 l X kPa-1 at 2-3 Hz; this change was primarily caused by the frequency-dependent behavior of chest wall compliance.     

Pleural pressure as a function of body position in rabbits

Pleural pressure was measured at end expiration in spontaneously breathing anesthetized rabbits. A liquid-filled capsule was implanted into a rib to measure pleural liquid pressure with minimal distortion of the pleural space. Capsule position relative to lung height was measured from thoracic radiographs. Measurements were made when the rabbits were in the prone, supine, right lateral, and left lateral positions. Average lung heights in the prone and supine positions were 4.21 +/- 0.58 and 4.42 +/- 0.51 (SD) cm, respectively (n = 7). Pleural pressure was -2.60 +/- 1.87 (SD) cmH2O at 50.2 +/- 7.75% lung height in the prone position and -3.10 +/- 1.22 cmH2O at 51.4 +/- 6.75% lung height in the supine position. There was no difference between the values recorded in the prone and supine positions. Placement of the capsule into the right or left chest had no effect on the magnitude of the pleural pressure recorded in rabbits in right and left lateral recumbency (n = 12). Measurements over the nondependent lung were repeatable when rabbits were turned between the right and left lateral positions. Lung height in laterally recumbent rabbits averaged 4.55 +/- 0.52 (SD) cm.     

Lung and chest wall impedances in the dog: effects of frequency and tidal volume.

Dependences of the mechanical properties of the respiratory system on frequency (f) and tidal volume (VT) in the normal ranges of breathing are not clear. We measured, simultaneously and in vivo, resistance and elastance of the total respiratory system (Rrs and Ers), lungs (RL and EL), and chest wall (Rcw and Ecw) of five healthy anesthetized paralyzed dogs during sinusoidal volume oscillations at the trachea (50-300 ml, 0.2-2 Hz) delivered at a constant mean lung volume. Each dog showed the same f and VT dependences. The Ers and Ecw increased with increasing f to 1 Hz and decreased with increasing VT up to 200 ml. Although EL increased slightly with increasing f, it was independent of VT. The Rcw decreased from 0.2 to 2 Hz at all VT and decreased with increasing VT. Although the RL decreased from 0.2 to 0.6 Hz and was independent of VT, at higher f RL tended to increase with increasing f and VT (i.e., as peak flow increased). Finally, the f and VT dependences of Rrs were similar to those of Rcw below 0.6 Hz but mirrored RL at higher f. These data capture the competing influences of airflow nonlinearities vs. tissue nonlinearities on f and VT dependence of the lung, chest wall, and total respiratory system. More specifically, we conclude that 1) VT dependences in Ers and Rrs below 0.6 Hz are due to nonlinearities in chest wall properties, 2) above 0.6 Hz, the flow dependence of airways resistance dominates RL and Rrs, and 3) lung tissue behavior is linear in the normal range of breathing.     

Rib cage vs. abdominal displacement in dogs during forced oscillation to 32 Hz

Allen et al. (J. Clin. Invest. 76: 620-629, 1985) reported that during oscillatory forcing the base of isolated canine lungs distends preferentially relative to the apex as frequency and tidal volume increase. The tendency toward such nonuniform phasic lung distension might influence phasic displacement of the rib cage (RC) relative to the abdomen (ABD). To test this hypothesis we measured RC and ABD displacement in four anesthetized dogs during forced oscillation. Sinusoidal volume changes were delivered through a tracheostomy at 1-32 Hz and measured by body plethysmography. RC and ABD displacements were measured by inductive plethysmography. During oscillation with air at fixed tidal volumes (10-80 ml) RC, normalized to unity at 1 Hz, increased to 2.06-2.22 at 8 Hz (P less than 0.001) and then decreased to 1.06-1.35 (P less than 0.0025) at 32 Hz. ABD, normalized to unity at 1 Hz, was 1.12-1.16 at 4 Hz (P less than 0.001) and decreased to 0.12-0.14 at 32 Hz (P less than 0.001). Displacement of ABD relative to RC did not increase systematically with increasing tidal volume during sinusoidal forcing at any frequency. Thus we found no discernible influence of nonuniform phasic lung distension on chest wall behavior. We infer that in the dog the nonuniform mechanical behavior of the chest wall dominates the nonuniform (but opposing) mechanical tendency of the lung.     

Comparison of lung sound transducers using a bioacoustic transducer testing system.

Sensors used for lung sound research are generally designed by the investigators or adapted from devices used in related fields. Their relative characteristics have never been defined. We employed an artificial chest wall with a viscoelastic surface and a white noise signal generator as a stable source of sound to compare the frequency response and pulse waveform reproduction of a selection of devices used for lung sound research. We used spectral estimation techniques to determine frequency response and cross-correlation of pulses to determine pulse shape fidelity. The sensors evaluated were the Siemens EMT 25 C accelerometer (Siemens); PPG 201 accelerometer (PPG); Sony ECM-T150 electret condenser microphone with air coupler (air coupler; with cylindrical air chambers of 5-, 10-, and 15-mm diameter and conical air chamber of 10-mm diameter); Littman classic stethoscope head (Littman) connected to an electret condenser microphone; and the Andries Tek (Andries) electronic stethoscope. We found that the size and shape of the air coupler chamber to have no important effect on the detected sound. The Siemens, air coupler, and Littman performed similarly with relatively flat frequency responses from 200 to 1,200 Hz. The PPG had the broadest frequency response, with useful sensitivity extending to 4,000 Hz. The Andries' frequency response was the poorest above 1,000 Hz. Accuracy in reproducing pulses roughly corresponded with the high-frequency sensitivity of the sensors. We conclude that there are important differences among commonly used lung sound sensors that have to be defined to allow the comparison of data from different laboratories.     

Regional blood flow to canine parietal pleura and internal intercostal muscle

Transcapillary Starling forces in the parietal pleura and the underlying interstitium may potentially contribute to the exchange of fluid across this barrier. However, the extent of blood flow to the parietal pleura has not been measured. Thus, using standard microsphere techniques, we compared blood flow to the parietal pleura, including the subpleural interstitium, with blood flow to the adjacent internal intercostal muscle, as well as with flows to other serous tissues, including mediastinal pleura, pericardium, and parietal peritoneum, in anesthetized dogs that were either breathing spontaneously (n = 9) or ventilated to control arterial PCO2 (n = 5). Blood flow (ml.min-1.g-1) was measured after 20 min of equilibration in four successive body positions: right lateral decubitus, supine, left lateral decubitus, and prone. Overall, flow to parietal pleura was not different in spontaneous [1.07 +/- 0.14 (SE)] and mechanically ventilated animals (0.74 +/- 0.11). Flow to the internal intercostal muscle was significantly less than pleural blood flow, averaging 0.24 +/- 0.03 and 0.16 +/- 0.03 in the same groups, although again there was no effect of ventilation mode. Blood flow to other serous tissues in the thoracic cavity, specifically the mediastinal pleura (0.67 +/- 0.14) and pericardium (0.88 +/- 0.22), was similar to parietal pleural flow, whereas that to the parietal peritoneum was an order of magnitude lower (0.09 +/- 0.02, P less than 0.05). Changing body position had no effect on blood flow to any of the sampled tissues. Blood flow to the dorsal aspect of the chest wall muscle in spontaneously breathing animals tended to be greater than that to lateral or ventral portions of the chest wall.(ABSTRACT TRUNCATED AT 250 WORDS)     

Specialization for underwater hearing by the tympanic middle ear of the turtle, Trachemys scripta elegans

Turtles, like other amphibious animals, face a trade-off between terrestrial and aquatic hearing. We used laser vibrometry and auditory brainstem responses to measure their sensitivity to vibration stimuli and to airborne versus underwater sound. Turtles are most sensitive to sound underwater, and their sensitivity depends on the large middle ear, which has a compliant tympanic disc attached to the columella. Behind the disc, the middle ear is a large air-filled cavity with a volume of approximately 0.5 ml and a resonance frequency of approximately 500 Hz underwater. Laser vibrometry measurements underwater showed peak vibrations at 500-600 Hz with a maximum of 300 μm s(-1) Pa(-1), approximately 100 times more than the surrounding water. In air, the auditory brainstem response audiogram showed a best sensitivity to sound of 300-500 Hz. Audiograms before and after removing the skin covering reveal that the cartilaginous tympanic disc shows unchanged sensitivity, indicating that the tympanic disc, and not the overlying skin, is the key sound receiver. If air and water thresholds are compared in terms of sound intensity, thresholds in water are approximately 20-30 dB lower than in air. Therefore, this tympanic ear is specialized for underwater hearing, most probably because sound-induced pulsations of the air in the middle ear cavity drive the tympanic disc.