Biomedical subjects

G M Barnas

Publications and source records attributed to G M Barnas.

At least 73 records · Page 4Linked to original sources

PubMed1989

Chest wall impedance partitioned into rib cage and diaphragm-abdominal pathways.

We measured chest wall "pathway impedances" (ratios of pressure changes to rates of volume displacement at the surface) with esophageal and gastric balloons and inductance plethysmographic belts around the rib cage and abdomen during forced volume oscillations (5% vital capacity, 0.5-4 Hz) at the mouth of five relaxed, seated subjects. Volume displacements of the total chest wall surface, measured by summing the rib cage and abdominal signals, approximated measurements using volume-displacement, body plethysmography over the entire frequency range. Resistance (R) and elastance (E) of the diaphragm-abdomen pathway were several times greater than those of the rib cage pathway, except at the highest frequencies where diaphragm-abdominal E was small. R and E of the diaphragm-abdomen pathway and of the rib cage pathway showed the same frequency dependencies as that of the total chest wall: R decreased markedly as frequency increased, and E (especially in the diaphragm-abdomen) decreased at the highest frequencies. These results suggest that the chest wall can be reasonably modeled, over the frequency range studied, as a system with two major pathways for displacement. Each pathway seems to exhibit behavior that reflects nonlinear, rate-independent dissipation as well as viscoelastic properties. Impedances of these pathways are useful indexes of changes in chest wall mechanical behavior in different situations.

Abdomen↗

PubMed1989

Impedance of the chest wall during sustained respiratory muscle contraction.

We measured total chest wall impedance (Zw), "pathway impedances" of the rib cage (Zrcpath), and diaphragm-abdomen (Zd-apath), and impedance of the belly wall including abdominal contents (Zbw+) in five subjects during sustained expiratory (change in average pleural pressure [Ppl] from relaxation = 10 and 20 cmH2O) and inspiratory (change in Ppl = -10 and -20 cmH2O) muscle contraction, using forced oscillatory techniques (0.5-4 Hz) we have previously reported for relaxation (J. Appl. Physiol. 66: 350-359, 1989). Chest wall configuration and mean lung volume were kept constant. Zw, Zrcpath, Zd-apath, and Zbw+ all increased greatly at each frequency during expiratory muscle contraction; increases were proportional to effort. Zw, Zrcpath, and Zd-apath increased greatly during inspiratory muscle contraction, but Zbw+ did not. Resistances and elastances calculated from each of the impedances showed the same changes during muscle contraction as the corresponding impedances. Each of the resistances decreased as frequency increased, independent of effort; elastances generally increased with frequency. These frequency dependencies were similar to those measured in relaxed or tetanized isolated muscle during sinusoidal stretching (P.M. Rack, J. Physiol. Lond. 183: 1-14, 1966). We conclude that during respiratory muscle contraction 1) chest wall impedance increases, 2) changes in regional chest wall impedances can be somewhat independent, depending on which muscles contract, and 3) increases in chest wall impedance are due, at least in part, to changes in the passive properties of the muscles themselves.

Adult↗

PubMed1989

Amplitude dependency of regional chest wall resistance and elastance at normal breathing frequencies.

Current methods for measurement of chest wall properties assume that resistance (R) and elastance (E) are independent of the volume breathed. In six healthy subjects relaxed at functional residual capacity, we measured total and regional R and E of the chest wall within the range of normal breathing frequencies (0.2 to 0.6 Hz) and tidal volumes (250 to 750 ml), using volume forcing at the mouth as previously described. With these methods, esophageal and gastric pressures are compared with surface displacements measured with inductance plethysmographic belts to calculate R and E of rib cage and diaphragm-abdomen "pathways." Rib cage R and E were 25 to 30% higher than that of the total chest wall at each frequency and volume, whereas diaphragm-abdomen R and E were at least five times higher. R of the chest wall and each of the pathways decreased by about 70% with increasing frequency and by about 30% with increasing tidal volume. E of the chest wall and each of the pathways also decreased by about 30% with increasing tidal volume but was independent of frequency in this range. These results are consistent with nonlinear, viscoplastic models presented elsewhere. We conclude that: (1) despite the great structural differences between the rib cage and diaphragm-abdomen, each exhibits nonlinear behavior similar to that of the total chest wall; (2) chest wall R and E depend importantly on frequency and tidal volume.

Adult↗

PubMed1987

Deposition and phagocytosis of inhaled particles in the gas exchange region of the duck, Anas platyrhynchos.

Little is known about the fate of inhaled aerosol particles in birds; even the anatomical location of phagocytic cells within the lungs has yet to be clearly demonstrated. We exposed 2 anesthetized, spontaneously breathing ducks to a non-toxic iron oxide aerosol (aerodynamic mass mean diameter = 0.18 micron; 460 mg/m3) for 1.75 h and 2 awake, resting ducks to less concentrated aerosol (38 mg/m3) for 6 h on two consecutive days. All 4 ducks were sacrificed 24 h after the end of the last exposure. Their lungs, as well as the lungs from a control duck not exposed to the aerosol, were fixed in situ by insufflation of osmium tetroxide vapor or by intravascular perfusion. Then samples of the gas exchange region were examined with a transmission electron microscope. We found iron oxide particles: trapped within the trilaminar substance that is unique to avian lungs and coats the atria and infundibula; within epithelial cells of the atria and initial portions of the infundibula; and within interstitial macrophages. Only occasionally, small amounts of particles were found in the air capillaries. We conclude that both epithelial cells and interstitial macrophages can phagocytize particles in avian lungs, and that there is some convective transport of aerosol to the atria and the initial portions of the infundibula.

Animals↗

PubMed1987

Inspiratory aerodynamic valving in goose lungs depends on gas density and velocity.

The non-reversing gas flow pattern in the avian lung has been attributed to 'aerodynamic valves'. A fundamental property of all aerodynamic valves is their dependence on inertial forces in the gas stream: sufficient reduction of inertial forces will cause aerodynamic valves to fail. If valving in the avian lung is aerodynamic, it should fail when gas stream momentum is reduced. We tested the dependence of the inspiratory valves in the goose lung on gas density and gas flow velocity. A bolus of tracer gas was placed in the tracheal cannula during an end-expiratory pause. Tracer gas appearance in a cranial air sac during the following inspiration and pause was used to deduce failure of the 'inspiratory valve' in cyclically ventilated geese. Little or no tracer entered the sac under control conditions, which approximated resting breathing, indicating highly effective valving. Lower flow rate or lower gas density caused increased tracer appearance, indicating valve failure. These results demonstrate the importance of gas inertial forces to normal valve function, and are direct evidence for the aerodynamic nature of the avian inspiratory valve.

Animals↗

PubMed1987

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.

Adult↗

PubMed1986

Cardiorespiratory responses to shivering in vagotomized pigeons during normoxia and hypoxia.

We measured respiratory, cardiovascular and blood gas responses to shivering during normoxia and hypoxia in five bilaterally, cervically vagotomized pigeons and compared these data with those previously reported in pigeons with intact vagi (Gleeson et al. 1986). Such neural section in birds denervates, among other receptors, the carotid bodies and intrapulmonary chemoreceptors. Normoxic breathing frequency (fR) and ventilation (VE) were decreased after vagotomy. Intact pigeons showed increases in oxygen consumption (VO2), tidal volume (VT), fR and VE during shivering. Vagotomized pigeons showed similar though slightly smaller increases in fR, VO2 and VE during shivering, but VT did not change. Normoxic heart rate was greater after vagotomy and was increased during shivering as in intact pigeons. Mean arterial blood pressure (MBPa) and stroke volume were not affected by vagotomy or shivering. At the onset of shivering both intact and vagotomized pigeons exhibited immediate increases in ventilation and heart rate. Exposure of vagotomized pigeons to hypoxic gas (fractional inspired oxygen concentration, FIO2 = 0.12) during cooling completely abolished shivering electromyogram (EMG) activity. In contrast, shivering in intact pigeons was not completely inhibited until the FIO2 fell below 0.10. We conclude that bilateral, cervical vagotomy in the pigeon causes hypoventilation and tachycardia during normoxia, but that these denervated birds are still able to rapidly effect cardiorespiratory adjustments to shivering. It is suggested that these responses are mediated mainly via afferent feedback from the shivering muscles. Hypoxia inhibits shivering in both intact and vagotomized birds and the mechanism is probably related to the reduced O2 delivery to the central structures that integrate thermoregulatory demand and coordinate appropriate responses.

Animals↗

PubMed1986

The effects of hypoxia on the metabolic and cardiorespiratory responses to shivering produced by external and central cooling in the pigeon.

Respiratory, cardiovascular and blood gas responses of pigeons to spinal cord cooling (36 +/- 1 degrees C), to ambient cooling (Ta = 5 degrees C) and to simultaneous spinal cord and ambient cooling were measured at three different levels of fractional inspired oxygen concentration (FIO2 = 0.209, 0.10 and 0.07). Shivering and the 'extra' VO2 provoked by ambient and/or spinal cord cooling were more or less reduced during hypoxic exposure depending on the intensity of cold stress and hypoxic states. At FIO2 = 0.10 shivering was markedly reduced and sometimes inhibited, whereas at FIO2 = 0.07 any pattern of cold tremor was inhibited. The accompanying cardiorespiratory responses were similar to those of thermoneutral controls exposed to the same FIO2. The amount by which VO2 was reduced in the pigeons exposed to hypoxia during ambient and/or spinal cord cooling was correlated, at both levels of hypoxia, to the thermoregulatory VO2 (viz. the 'extra' VO2 produced by cooling) prior to exposure to the hypoxic gas. The effect of hypoxia on shivering and associated cardiorespiratory adjustments was rapid and was completely reversible on return to air. We conclude that the thermoregulatory system in pigeons is sensitive to hypoxia, as is the case for mammals. The FIO2 that begins to inhibit thermoregulatory and metabolic responses to cold is lower in birds, perhaps as a result of the better ability of the bird to increase intrapulmonary gas and blood O2 convective transports when exposed to hypoxic gas.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1986

Effect of bilateral vagotomy on arterial acid-base stability during panting in the pigeon.

Bilateral, cervical vagotomy denervates, among other receptors, the known peripheral chemoreceptors in birds. To test the importance of afferent vagal input to cardiorespiratory control during thermal panting, we measured responses to an increase in body temperature (Tb) induced by ambient heating in 6 bilaterally, cervically vagotomized pigeons. These responses were compared with those we previously reported in intact pigeons (control animals). At thermoneutral conditions, respiratory frequency (fR) was lower after vagotomy compared to controls, and PaCO2 was higher. During increases in Tb in both control and vagotomized pigeons, fR, PaO2, pHa, heart rate and oxygen consumption increased, and PaCO2 decreased. However, fR rose less, PaCO2 decreased more, and pHa increased more in the vagotomized pigeons than in controls. All three were more variable than in controls. Heart rate and blood pressure were higher than controls; blood pressure was more variable. We conclude that bilateral, cervical vagotomy compromises the ability of pigeons to maintain stable respiratory and cardiovascular responses to hyperthermia.

Acid-Base Equilibrium↗

PubMed1986

Pulmonary afferent activity during high-frequency ventilation at constant mean lung volume.

We recorded the responses of 21 slowly adapting pulmonary stretch receptors (PSRs) and 8 rapidly adapting pulmonary stretch receptors (RARs) from the vagi of anesthetized open-chest dogs to high-frequency ventilation (HFV) at 15 Hz, at constant mean end-expiratory lung volume, and constant end-tidal PCO2. HFV applied in this way has been shown to prolong expiration. The responses of pulmonary afferents during HFV at constant mean volume have not been described. In the present experiments, receptor discharge during HFV was compared with that during the end-expiratory pause of normal-frequency ventilation. Average PSR discharge increased when HFV was applied, although not all PSRs exhibited increases. RARs were generally silent during normal and high-frequency ventilation at functional residual capacity and above. However, at low lung volumes, RAR discharge increased greatly when HFV was applied. We conclude that PSR discharge is increased during HFV in the absence of increased lung volume and that increases in PSR discharge during HFV are sufficient to explain the reflex that prolongs expiration in dogs.

Adaptation, Physiological↗

PubMed1986

Cardiorespiratory responses to hypoxia in intact and bilaterally vagotomized pigeons.

Bilateral, cervical vagotomy in birds denervates, among other receptors, the carotid bodies. To test whether such neural section removes sensitivity to hypoxia, we measured respiratory, cardiovascular, and blood gas responses to hypoxia at 84-, 70-, and 49-Torr inspiratory O2 partial pressure (PIO2) in five pigeons with intact vagi and in five bilaterally, cervically vagotomized pigeons. Normoxic respiratory frequency (fresp) and expiratory flow rate (VE) were decreased after vagotomy. Intact pigeons showed large increases in VE in response to hypoxia, effected mostly by increases in fresp. VE also increased greatly in response to hypoxia in vagotomized pigeons, but increases were largely the result of tidal volume. O2 consumption, CO2 production, and respiratory exchange ratio increased slightly in all pigeons during hypoxia. Normoxic heart rate was greater after vagotomy; cardiac output increased in all pigeons in response to hypoxia, but stroke volume increased only in intact pigeons. During normoxia, arterial and mixed venous O2 partial pressure, O2 concentration, and pH were lower and arterial and mixed venous CO2 partial pressure was higher, after vagotomy. In all pigeons during hypoxia, arterial and mixed venous O2 and CO2 partial pressure and O2 concentration decreased and arterial and mixed venous pH increased; changes were roughly parallel in intact and vagotomized pigeons. The arteriovenous O2 concentration differences during normoxia and hypoxia were similar in all pigeons. We conclude that bilateral, cervical vagotomy in the pigeon causes hypoventilation and tachycardia during normoxia, but strong respiratory and cardiovascular responses to hypoxia are still present.

Animals↗

PubMed1985

Intrapulmonary chemoreceptor control of ventilatory movements in the self-ventilating chicken.

The importance of intrapulmonary chemoreceptors (IPC), sensitive to PCO2 in the lung, in the control of ventilatory movements is yet to be demonstrated in the self-ventilating bird. We distinguished between the effects of PCO2 on IPC and on extrapulmonary CO2-sensitive receptors (EPC) in anaesthetized cockerels by denervating IPC in the right lung, ligating the left pulmonary artery and changing PICO2. Left IPC were thus exposed to a combination of PCO2 from inspired gas and dead space, while EPC were exposed to greatly increased arterial PCO2 resulting from the ventilation-perfusion inequality. At 0 Torr PICO2, steady state ventilatory depth and frequency did not change (P greater than 0.5) after the ligation, although PaCO2 rose by 12.2 +/- 1.7 Torr. After the ligation, ventilatory movements were more sensitive to increasing PICO2. Tracheostomy, which results in a greater decrease in PCO2 in the innervated lung after ligation, produced greater effects. We conclude that these responses were due to the strong controlling influence of IPC on ventilatory movements in the self-ventilating cockerel.

Analysis of Variance↗

PubMed1985

Respiratory and cardiovascular responses of the exercising chicken to spinal cord cooling at different ambient temperatures. I. Cardiovascular responses and blood gases.

We measured oxygen consumption (VO2), heart rate (HR), stroke volume (SV), cardiac output (CO) and mean arterial blood pressure (MBPa) of chickens during 15 min treadmill exercise at 0.5 ms-1 and 0.8 ms-1 at thermoneutral (23 degrees C), low (9 degrees C) and high (34 degrees C) ambient temperature (Ta); the vertebral canal was cooled to 34 degrees C during the middle 5 min of each exercise period. PO2, PCO2, pH and oxygen content (CO2) of the arterial and mixed venous blood were also measured. VO2 during exercise was not significantly affected by Ta. Spinal cord cooling produced definite increases in VO2, CO and SV during 0.5 ms-1 exercise at 9 degrees C; otherwise, effects of spinal cord cooling were not significant. HR, SV and CO were all linearly related to VO2; these relationships were unaffected by spinal cord cooling or Ta. Blood pressure did not increase during exercise. PaCO2 and P-vCO2 did not increase significantly during exercise. The arterial-venous CO2 difference was increased by exercise only at 34 degrees C. The chickens generally hyperventilated at 34 degrees C Ta compared to the other Ta values. No consistent effect on blood gases or on pH and CO2 of the blood could be attributed to spinal cord cooling.

Animals↗

PubMed1985

Respiratory and cardiovascular responses of the exercising chicken to spinal cord cooling at different ambient temperatures. II. Respiratory responses.

We measured oxygen consumption (VO2), carbon dioxide production (VCO2), minute volume (VE), respiratory frequency (f) and tidal volume (VT) of chickens during 15 min treadmill exercise at 0.5 ms-1 and 0.8 ms-1 at thermoneutral (23 degrees C), low (9 degrees C) and high (34 degrees C) ambient temperature (Ta); the vertebral canal was cooled to 34 degrees C during the middle 5 min of each exercise period. Temperatures of the vertebral canal (TVC) and rectum (Tre) were also measured. Exercise at 0.5 ms-1 caused increases in O2 consumption, CO2 production, minute volume and tidal volume compared to resting controls at each Ta. Minute volume and respiratory frequency were higher and tidal volume was lower in birds exercising at 34 degrees C than at 23 or 9 degrees C. Spinal cord cooling during exercise (0.5 ms-1) at 9 degrees C caused further increases in O2 consumption, tidal volume and respiratory frequency almost equivalent to those produced by an increase in the running speed to 0.8 ms-1. Spinal cord cooling during exercise (0.5 ms-1) at 23 degrees C did not significantly affect O2 consumption, CO2 production, minute volume, tidal volume or respiratory frequency. Spinal cord cooling during exercise (0.5 ms-1) at 34 degrees C did not affect O2 consumption or CO2 production, but caused decreases in minute volume and respiratory frequency and an increase in tidal volume. We conclude that the domestic fowl exhibits spinal thermosensitivity during exercise, although these responses appear to be smaller than those previously reported for the resting bird. Decreased external temperature potentiates the effects of spinal cord cooling during exercise.

Animals↗

PubMed1984

Cardiovascular and blood gas changes during panting responses induced by ambient or spinal cord heating in the pigeon.

We measured respiratory frequency (fR), oxygen consumption (VO2), cardiovascular responses and arterial and mixed venous PCO2, PO2, pH and CO2 in six pigeons during hyperthermia caused by ambient heating (increase in body temperature = 1 degrees C) and during heating of the spinal cord alone (increase in vertebral canal temperature = 3 degrees C). Spinal cord heating caused an increase in fR to 546 min-1 (+/- 13 min-1 SE) and increases in VO2, heart frequency (fH) and cardiac output (CO); PaCO2 and PVCO2 decreased 3.4 and 4.6 torr, respectively, while PaCO2 increased 6.8 torr. fR during ambient heating was 489 +/- 36 min-1; cardiovascular and blood gas changes were, generally, in the same direction as those during spinal cord heating but of lesser magnitude. In six other pigeons, we characterized fR, VO2, cardiovascular and blood gas changes during a 4 degrees C rise in body temperature caused by increased ambient temperature. Those data showed that with increasing hyperthermia fR increased rapidly, though not stepwise, to a maximum while VO2, fH, CO, PaO2, pHa and the arterial-venous CO2 difference all gradually increased; PaCO2 and PVCO2 gradually decreased. We conclude that, generally, whole body heating by increased ambient temperature and heating of the spinal cord alone produce the same responses and that these responses are dependent on the magnitude of the heat stimulation.

Animals↗

PubMed1983

Interaction of temperature with extra- and intrapulmonary chemoreceptor control of ventilatory movements in the awake chicken.

Several studies in artificially ventilated, anesthetized birds with opened thoracoabdominal cavities have shown that intrapulmonary chemoreceptors (IPC) sensitive to CO2 contribute to the control of ventilatory movements. Increasing colonic temperature (Tc) has been shown to increase depth and decrease frequency of ventilatory movements if PaCO2 is held constant at less than 35 torr in awake and anesthetized, artificially ventilated cockerels. The relative importances, though, of IPC and of extrapulmonary CO2-sensitive chemoreceptors (EPC) in controlling ventilation in the awake or hyperthermic bird is unknown. We dissociated the PCO2 affecting IPC and EPC in awake cockerels by ligating the left pulmonary artery, denervating the IPC in the right lung and artificially ventilating each lung separately. We found, that at constant PaCO2, ventilatory movements increased in depth and decreased in frequency with: (1) increasing PICO2 to the innervated, non-perfused lung (PipcCO2); and (2) increasing Tc. Similar responses were observed with increasing PaCO2 or Tc during constant PipcCO2. Multiple regression analyses show that IPC and EPC have about equal controlling influences on ventilatory movements in the awake and hyperthermic cockerel.

Alkalosis, Respiratory↗

PubMed1983

Effect of temperature on the CO2 sensitivity of avian intrapulmonary chemoreceptors.

We determined linear regressions of discharge frequency on ln PCO2 of 23 intrapulmonary chemoreceptors (IPC) from eight hyperthermic, adult cockerels. At low PCO2, IPC in hyperthermic cockerels discharged slower than IPC measured in euthermic cockerels; above 25 torr PCO2, however, they discharged faster than euthermic IPC. Thus, IPC were less sensitive to PCO2 during hyperthermia. We calculate that a 1 degree C increase in the temperature of the lung (TL) causes the slope of the linear regression of discharge frequency on ln PCO2 to be less negative by 1.5 +/- 0.5 imp (sec X ln PCO2)-1 and that, for any increase in TL above normal (41.5 degrees C), the average IPC discharge frequency equals (-10.7 + 1.5 (TL -41.5] X (ln (PCO2/25.0] + 3.7. This relationship may be partly responsible for the increased tidal volume and decreased respiratory frequency observed when body temperature increases during constant PaCO2.

Alkalosis, Respiratory↗

PubMed1981

The effect of CO2 and temperature on respiratory movements in the chicken.

We studied the effect of increasing colonic temperature (Tc) on respiratory amplitude and frequency at different levels of PICO2 in anesthetized, unidirectionally ventilated cockerels. We also evaluated the relationship between PICO2 and PaCO2. Increased PaCO2 augmented respiratory amplitude and decreased frequency at every Tc. Respiratory amplitude increased as Tc rose from 41 to 45 degrees C at each level of PaCO2. During the same rise in Tc, respiratory frequency decreased at the low PaCO2 seen in awake, panting cockerels but increased at eucapnic PaCO2. Tc had no effect on frequency at high PaCO2. Values for respiratory frequency of unidirectionally ventilated cockerels at given Tc and PaCO2 predict those of awake cockerels. We conclude that amplitude of breathing increases in acute hyperthermia unless accompanied by hypocapnia and that without hypocapnia maximal panting frequencies cannot be reached.

Animals↗