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Biomedical subjects

J Solway

Publications and source records attributed to J Solway.

At least 91 records · Page 5Linked to original sources
PubMed1988

Properties of steady maximal expiratory flow within excised canine central airways.

Using our transistor model of the lung during forced expiration (J. Appl. Physiol. 62: 2013-2025, 1987), we recently predicted that 1) axially arranged choke points can exist simultaneously during forced expiration with sufficient effort, and 2) overall maximal expiratory flow may be relatively insensitive to nonuniform airways obstruction because of flow interdependence between parallel upstream branches. We tested these hypotheses in excised central airways obtained from five canine lungs. Steady expiratory flow was induced by supplying constant upstream pressure (Pupstream = 0-16 cmH2O) to the bronchi of both lungs while lowering pressure at the tracheal airway opening (16 to -140 cmH2O). Intra-airway pressure profiles obtained during steady maximal expiratory flow disclosed a single choke point in the midtrachea when Pupstream was high (2-16 cmH2O). However, when Pupstream was low (0 cmH2O), two choke sites were evident: the tracheal site persisted, but another upstream choke point (main carina or both main bronchi) was added. Flow interdependence was studied by comparing maximal expiratory flow through each lung before and after introduction of a unilateral external resistance upstream of the bronchi of one lung. When this unilateral resistance was added, ipsilateral flow always fell, but changes in flow through the contralateral lung depended on the site of the most upstream choke. When a single choke existed in the trachea, addition of the external resistance increased contralateral flow by 38 +/- 28% (SD, P less than 0.003). In contrast, when the most upstream choke existed at the main carina or in the bronchi, addition of the external resistance had no effect on contralateral maximal expiratory flow.(ABSTRACT TRUNCATED AT 250 WORDS)

Airway Resistance↗
PubMed1988

Pressure, flow, and density relationships in airway models during constant-flow ventilation.

Adequate CO2 elimination and normal arterial PCO2 levels can be maintained in dogs during apnea by delivering a continuous flow of inspired gas at high flow rate (1-3 l.min-1.kg-1) through tubes placed in the main-stem bronchi. However, during constant-flow ventilation (CFV) the mean alveolar pressure is increased, causing increased lung volume despite low pressures in the trachea. We hypothesized that the increased dynamic alveolar pressures during CFV were due to momentum transfer from the high-velocity jet stream to resident gas in the lung. To test this, we simulated CFV in straight tubes and in a branched airway model to determine whether changes in gas flow rate (V), gas density (rho), and tube diameter (D) altered the pressure difference (delta P) between alveoli and airway opening in a manner consistent with that predicted by conservation of momentum. Momentum analysis predicts that delta P should vary with V2, whereas measurements yielded a dependence of V1.69 in branched tubes and V1.9 in straight tubes. Substitution of heliox (80% He-20% O2) for air significantly reduced lung hyperinflation during CFV. As predicted by momentum transfer, delta P varied with rho 1.0. Momentum analysis also predicts that delta P should vary with D-2.0, whereas measurements indicated a dependence on D-2.02. The influence of V and rho on depth of penetration of the jet down the airway was explored in a straight tube model by varying the flow rate and gas used. The influence of geometry on penetration was measured by changing the ratio of jet-to-airway tube diameters.(ABSTRACT TRUNCATED AT 250 WORDS)

Models, Biological↗
PubMed1988

Bronchoconstriction elicited by isocapnic hyperpnea in guinea pigs.

We demonstrated spontaneous self-limited bronchoconstriction after eucapnic dry gas hyperpnea in 22 anesthetized, mechanically ventilated guinea pigs pretreated with propranolol (1 mg/kg iv). Eucapnic hyperpnea "challenges" of room temperature dry or humidified gas (5% CO2-95% O2) were performed by mechanically ventilating animals (150 breaths/min, 3-6 ml tidal volume) for 5 min. During a "recovery" period after hyperpnea, animals were returned to standard ventilation conditions (6 ml/kg, 60 breaths/min, 50% O2 in air, fully saturated at room temperature). After dry gas hyperpnea (5 ml, 150 breaths/min), respiratory system resistance (Rrs) increased in the recovery period by 7.7-fold and dynamic compliance (Cdyn) decreased by 79.7%; changes were maximal at approximately 3 min posthyperpnea and spontaneously returned to base line in 10-40 min. This response was markedly attenuated by humidification of inspired air. Four consecutive identical dry air challenges resulted in similar posthyperpnea responses in four animals. Increasing the minute ventilation during hyperpnea (by varying tidal volume from 3 to 6 ml) caused increased bronchoconstriction in a dose-dependent fashion in six animals. Neither vagotomy nor atropine altered the airway response to dry gas hyperpnea. We conclude that dry gas hyperpnea in anesthetized guinea pigs results in a bronchoconstrictor response that shares five similar features with hyperpnea-induced bronchoconstriction in human asthma: 1) time course of onset and spontaneous resolution, 2) diminution with humidification of inspired gas, 3) reproducibility on consecutive identical challenges, 4) stimulus-response relationship with minute ventilation during hyperpnea, and 5) independence of parasympathetic neurotransmission.

Airway Resistance↗
PubMed1988

Lobar contribution to VA/Q inequality during constant-flow ventilation.

Previous studies have shown that normal arterial PCO2 can be maintained during apnea in anesthetized dogs by delivering a continuous stream of inspired ventilation through cannulas aimed down the main stem bronchi, although this constant-flow ventilation (CFV) was also associated with a significant increase in ventilation-perfusion (VA/Q) inequality, compared with conventional mechanical ventilation (IPPV). Conceivably, this VA/Q inequality might result from differences in VA/Q ratios among lobes caused by nonuniform distribution of ventilation, even though individual lobes are relatively homogeneous. Alternatively, the VA/Q inequality may occur at a lobar level if those factors causing the VA/Q mismatch also existed within lobes. We compared the efficiency of gas exchange simultaneously in whole lung and left lower lobe by use of the multiple inert gas elimination technique in nine anesthetized open-chest dogs. Measurements of whole lung and left lower lobe gas exchange allowed comparison of the degree of VA/Q inequality within vs. among lobes. During IPPV with positive end-expiratory pressure, arterial PO2 and PCO2 (183 +/- 41 and 34.3 +/- 3.1 Torr, respectively) were similar to lobar venous PO2 and PCO2 (172 +/- 64 and 35.7 +/- 4.1 Torr, respectively; inspired O2 fraction = 0.44 +/- 0.02). Switching to CFV (3 l.kg-1.min-1) decreased arterial PO2 (112 +/- 26 Torr, P less than 0.001) and lobar venous PO2 (120 +/- 27 Torr, P less than 0.01) but did not change the shunt measured with inert gases (P greater than 0.5).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1988

Dissociation of temperature-gradient and evaporative heat loss during cold gas hyperventilation in cold-induced asthma.

We examined temperature-gradient and evaporative energy losses during cold gas inhalation challenges in patients with exercise-induced asthma by using gases with similar water-carrying capacities but significantly different volume heat capacities. Seven subjects were asked to hyperventilate mixtures of 80% helium/20% oxygen (HeO2) or 80% sulfur hexafluoride/20% oxygen (SF6O2) for 5 min at a fixed target minute ventilation of 20 x FEV1 and an inspired gas temperature of 0 degrees C. Each subject equilibrated his or her lungs with the appropriate gas mixture prior to testing: PETCO2 and FIO2 were monitored and maintained at constant values (CO2 = 0.05; O2 = 0.20) by CO2 scrubbing and addition of compressed gas to the system. Gas composition, inspired and expired flow rates, and gas temperatures at the airway opening were recorded in real time using a computer-based data collection system that calculated respiratory heat loss on a per breath basis. Bronchoconstriction was quantitated using specific airway conductance measured before and serially after each challenge. The degree of bronchoconstriction correlated closely with evaporative respiratory heat loss (r = 0.658 p less than 0.05), but poorly with both temperature-gradient (r = 0.114, p greater than 0.20) and total (r = 0.268, p greater than 0.15) heat loss. These findings suggest that total respiratory heat loss is not the primary stimulus in exercise-induced asthma, and further suggest that total water loss, or focal heat/water loss, may be important in inducing bronchospasm in this subset of asthmatics.

Adult↗
PubMed1987

Partitioning of pulmonary resistance during constriction in the dog: effects of volume history.

We assessed the relative changes in airways and lung tissue with bronchoconstriction, and the changes in each during and following a deep inhalation (DI). We partitioned pulmonary resistance (RL) into airway (Raw) and tissue (Vtis) components using alveolar capsules in 10 anesthetized, paralyzed, and open-chested dogs ventilated sinusoidally with 350-ml breaths at 1 Hz. We made measurements before and during bronchoconstriction induced by vagal stimulation or inhalation of histamine or prostaglandin F2 alpha (PGF2 alpha), each of which decreased dynamic compliance by approximately 40%. With histamine and PGF2 alpha the rise in RL was predominantly due to Vtis. With vagal stimulation there was a relatively greater increase in Raw than Vtis. At higher lung volumes, Vtis increases offset falls in Raw, producing higher RL at these volumes before and during constriction with PGF2 alpha and histamine. During constriction with vagal stimulation, the fall in Raw with inflation overrode the rise in Vtis, resulting in a lower RL at the higher compared with the lower lung volume. The changes seen after a DI in the control and constricted states were due to alterations in tissue properties, both viscous and elastic. However, the relative hysteresis of the airways and parenchyma were equal, since Raw, our index of airway size, was unchanged after a DI.

Airway Resistance↗
PubMed1987

Interdependent regional lung emptying during forced expiration: a transistor model.

We recognized similarities between isovolume pressure-flow curves of the lung and emitter-collector voltage-current characteristics of bipolar transistors, and used this analogy to model expiratory flow limitation in a two-generation branching network with parallel nonhomogeneity. In this model, each of two bronchi empty parenchymal compliances through a common trachea, and each branch includes resistances upstream and downstream of a flow-limiting site. Properties of each airway are specified independently, allowing simulation of differences between the tracheal and bronchial generations and between the parallel bronchial paths. Simulations of four types of parallel asymmetry were performed: unilateral peripheral bronchoconstriction; unilateral central bronchoconstriction; asymmetric redistribution of parenchymal compliance; and unilateral alteration of the bronchial area-transmural pressure characteristic. Our results indicate that multiple axial choke points can exist simultaneously in a symmetric lung when large airway opening-pleural pressure gradients exist; despite severe nonhomogeneity of regional lung emptying, flow interdependence among parallel branches tends to maintain a near normal configuration of the overall maximal expiratory flow-volume (MEFV) curve throughout a large fraction of the vital capacity; and sudden changes of slope of the MEFV curve ("knees" or "bumps") may reflect choking in one branch in a nonuniform lung, but need not be obvious even when severe heterogeneity of lung emptying exists.

Airway Resistance↗
PubMed1987

Indirect assessment of mucosal surface temperatures in the airways: theory and tests.

We developed and tested a method, based on conduction heat transfer analysis, to infer airway mucosal temperatures from airstream temperature-time profiles during breath-hold maneuvers. The method assumes that radial conduction of heat from the mucosal wall to inspired air dominates heat exchange during a breath-hold maneuver and uses a simplified conservation of energy analysis to extrapolate wall temperatures from air temperature vs. time profiles. Validation studies were performed by simultaneously measuring air and wall temperatures by use of a retractable basket probe in the upper airways of human volunteers and intrathoracic airways of paralyzed intubated dogs during breath holding. In both protocols, a good correlation was demonstrated between directly measured wall temperatures and those calculated from adjacent airstream temperature vs. time profiles during a breath hold. We then calculated intrathoracic bronchial wall temperatures from breath-hold airstream temperature-time profiles recorded in normal human subjects after cold air hyperpnea at 30 and 80 l/min. The calculations show airway wall temperatures in the upper intrathoracic airways that are below core body temperature during hyperpnea of frigid air and upper thoracic airways that are cooler than more peripheral airways. The data suggest that the magnitude of local intrathoracic heat/water flux is not represented by heat/water loss measurements at the airway opening. Both the magnitude and locus of heat transport during cold gas hyperventilation vary with changes in inspired gas temperature and minute ventilation; both may be important determinants of airway responses.

Animals↗
PubMed1987

Bronchoconstrictor effects of leukotriene E4 in normal and asthmatic subjects.

The bronchoconstrictor activity of an aerosol of leukotriene E4(LTE4) was compared with that of histamine in 5 normal and in 6 asthmatic subjects to define the relative potency of LTE4 between the groups using 3 indices of airway response. The FEV1 and the flow rate measured at 30% of vital capacity from partial and maximal expiratory maneuvers (V30-P and V30-M) were measured. The geometric mean (GSEM) concentration of LTE4 required to reduce the V30-P by 30% was 0.30 (1.46) mM in the normal subjects, and 0.058 (1.63) in the asthmatic subjects; LTE4 was 39-fold more potent than histamine in the former and 14-fold in the latter group. Further, we observed that when normal and asthmatic subjects were compared at a degree of bronchoconstriction resulting in a 30% decrement in the V30-P after inhaling LTE4, there was a greater response in the asthmatic group than in the normal group of the accompanying change in the FEV1. The decrements in the FEV1 were not significantly different between the 2 groups after inhaling histamine. This study demonstrates that LTE4 is a potent bronchoconstrictor agonist in humans and suggests that airway responsiveness to this agonist differs substantially with the index of bronchoconstriction used for assessment of airway response.

Aerosols↗
PubMed1987

Distribution of airway contractile responses within the major diameter bronchi during exogenous bronchoconstriction.

The distribution of bronchoconstrictor responses within airway generations zero to 6 was studied by tantalum bronchography during exogenous bronchoconstriction with methacholine (MCh), prostaglandin F2 alpha (PGF2 alpha), norepinephrine (NE), and the thromboxane mimetic U-46619 [(15S)-hydroxyl-11 alpha,9 alpha-(epoxymethano)prosta-5Z, 13E-dienoic acid] in 12 mongrel dogs undergoing vagotomy and beta-adrenergic blockade. Dose-response curves to each agonist were generated in random order, and tantalum bronchograms and simultaneous measurements of pulmonary resistance (RL) and dynamic pulmonary compliance (Cdyn) were obtained at the plateau of the response of each dose of agonist after intravenous (iv) infusion. At 5 X 10(-7) mol/kg, NE (after beta-adrenergic blockade) caused an increase to 254 +/- 27.3%, PGF2 alpha to 368 +/- 50.0%, U-46619 to 522 +/- 98.5%, and MCh to 1,204 +/- 173% of baseline in RL. However, airway diameter changes within the major diameter airways varied substantially for each agonist. Methacholine caused substantial contraction in all airways. Neither NE nor U-46619 caused significant airway narrowing in generations zero or 1, although both agonists caused greater than 30% narrowing in sixth generation airways. Prostaglandin F2 alpha (5 X 10(-7) mol/kg) cause an increase in RL of greater than 350%; however, this was accompanied by an approximately 10% increase (dilation) in airway diameter in generation 1 through generation 4 airways and an approximate 25% narrowing in generation 6 airways. We demonstrate that both alpha-adrenergic agonists and thromboxane analog cause substantial bronchoconstriction in situ in the central air-ways of the lung.(ABSTRACT TRUNCATED AT 250 WORDS)

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗
PubMed1986

Expiratory flow limitation and dynamic pulmonary hyperinflation during high-frequency ventilation.

Dynamic hyperinflation of the lungs occurs during high-frequency oscillatory ventilation (HFOV) and has been attributed to asymmetry of inspiratory and expiratory impedances. To identify the nature of this asymmetry, we compared changes in lung volume (VL) observed during HFOV in ventilator-dependent patients with predictions of VL changes from electrical analogs of three potential modes of impedance asymmetry. In the patients, when a fixed oscillatory tidal volume was applied at a low mean airway opening pressure (Pao), which resulted in little increase in functional residual capacity, progressively greater dynamic hyperinflation was observed as HFOV frequency, (f) was increased. When mean Pao was raised so that resting VL increased, VL remained at this level during HFOV as f was increased until a critical f was reached; above this value, VL increased further with f in a fashion nearly parallel to that observed when low mean Pao was used. Three modes of asymmetric inspiratory and expiratory impedance were modeled as electrical circuits: 1) fixed asymmetric resistance [Rexp greater than Rinsp]; 2) variable asymmetric resistance [Rexp(VL) greater than Rinsp, with Rexp(VL) decreasing as VL increased]; and 3) equal Rinsp and Rexp, but with superimposed expiratory flow limitation, the latter simulated using a bipolar transistor as a descriptive model of this phenomenon. The fixed and the variable asymmetric resistance models displayed a progressive increase of mean VL with f at either low or high mean Pao. Only the expiratory flow limitation model displayed a dependence of dynamic hyperinflation on mean Pao and f similar to that observed in our patients. We conclude that expiratory flow limitation can account for dynamic pulmonary hyperinflation during HFOV.

Adult↗
PubMed1986

CO2 elimination by high-frequency oscillation: effects of vagosympathetic stimulation.

The effects of electrical stimulation of the vagi on gas transport mediated by high-frequency, low tidal volume ventilation (HFV) was examined in 10 anesthetized, paralyzed, propranolol-treated dogs. Gas transport efficiency was estimated by measuring the rate of CO2 removed from the lungs (Vco2) achieved during 45-s bursts of HFV applied before (control 1), during, and after (control 2) electrical stimulation of the transected vagi. During vagal stimulation the heart rate was maintained by electrical pacing. During the 15-s phase of vagal stimulation pulmonary impedance increased from 3.6 +/- 0.7 to 6.2 +/- 2.2 cmH2O X l-1 X s, and Vco2 increased. When the electrical stimulation of the vagi was stopped, impedance and Vco2 returned to prestimulation values. Vco2 was always higher during electrical stimulation of the vagi when HFV of a fixed volume was applied over a range of frequencies or when a fixed oscillation frequency was used over a range of tidal volumes. The effects of vagal stimulation on HFV-mediated gas transport were quite similar to the effects of moving the locations of the bias flow inlet and outlet into the lung such that tracheal volume was decreased by 20 ml, an amount equivalent to estimated change in control airway volume thought to occur during vagal stimulation. We simulated the effects of vagal stimulation and decreased tracheal volume on Vco2 by using a previously described model of HFV-mediated gas transport.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1986

Finite difference analysis of respiratory heat transfer.

A numerical computer model of heat and water transfer within the tracheobronchial tree of humans was developed based on an integral formulation of the first law of thermodynamics. Simulation results were compared with directly measured intraluminal airway temperature profiles previously obtained in normal human subjects, and a good correlation was demonstrated. The model was used to study aspects of regional pulmonary heat transfer and to predict the outcomes of experiments not yet performed. The results of these simulations show that a decrease in inspired air temperature and water content at fixed minute ventilation produces a proportionately larger increase in heat loss from extrathoracic airways relative to intrathoracic, whereas an increase in minute ventilation at fixed inspired air conditions produces the opposite pattern, with cold dry air penetrating further into the lung, and that changes in breathing pattern (tidal volume and frequency) at fixed minute ventilation and fixed inspiratory-to-expiratory (I/E) ratio do not affect local air temperature profiles and heat loss, whereas changes in I/E ratio at fixed minute ventilation do cause a significant change.

Asthma↗
PubMed1986

Circulatory heat sources for canine respiratory heat exchange.

We assessed the roles of the pulmonary and bronchial circulations as potential heat sources to the pulmonary airways during respiratory heat loss, by observing the changes in airstream temperature that accompanied temporary occlusion of the pulmonary or bronchial circulations. Baseline end-expiratory and end-inspiratory airstream temperatures were 35.4 +/- 0.2 degrees C (SEM) and 30.9 +/- 0.3 degrees C, respectively, among all trials. With occlusion of the lower lobe pulmonary arteries for 3 min ipsilateral end-expiratory and end-inspiratory airstream temperatures fell by 2.8 +/- 0.2 and 1.1 +/- 0.2 degrees C, respectively, during hyperpnea with room temperature air, and by 3.5 +/- 0.5 and 1.8 +/- 0.2 degrees C, respectively, during hyperpnea with frigid air. In marked contrast, interruption of the bronchial circulation for 3 min had no effect on airstream temperatures. These data indicate that under these conditions, the pulmonary circulation, but not the bronchial circulation, serves as an important local heat source for respiratory heat exchange within the pulmonary airways.

Animals↗
PubMed1985

Effect of bias flow rate on gas transport during high-frequency oscillatory ventilation.

Ventilatory support with low tidal volume, high-frequency oscillatory ventilation (HFOV) usually uses a bias flow system to provide fresh gas. Although the bias flow rates (Vbf) used previously have varied widely among experimental configurations, the precise role of the bias flow in HFOV-mediated gas transport has not been defined. We assessed the effect of bias flow rate on gas transport during HFOV by measuring CO2 removal rate (MCO2) in anesthetized, paralyzed dogs, using a wide range of bias flow rates (0.7-28.9 L X min-1). When a fixed tidal volume of 40 ml was applied at HFOV frequencies of 2-12 Hz, MCO2 was proportional to the time-averaged alveolar-bias flow CO2 concentration difference. Thus, when Vbf was reduced below a value which resulted in a substantial increase in bias flow CO2 concentration, MCO2 was reduced. These findings are consistent with a simple framework in which the relative magnitudes of the resistances to gas transport of the airways and of the bias flow (1/Vbf) determine the contribution of the bias flow rate to overall gas transport during HFOV. This relationship may be employed to assess the intra-airway contribution to HFOV-mediated gas transport at any bias flow rate, and may therefore allow comparison of results from experiments utilizing various bias flow rates.

Animals↗
PubMed1985

Thermal mapping of the airways in humans.

To characterize the intrathoracic thermal events that occur during breathing in humans, we developed a flexible probe (OD 1.4 mm) containing multiple thermistors evenly spaced over 30.2 cm, that could be inserted into the tracheobronchial tree with a fiberoptic bronchoscope. With this device we simultaneously recorded the airstream temperature at six points from the trachea to beyond the subsegmental bronchi in six normal subjects while they breathed ambient and frigid air at multiple levels of ventilation (VE). During quiet breathing of room air the average temperature ranged from 32.0 +/- 0.05 degrees C in the upper trachea to 35.5 +/- 0.3 degrees C in the subsegmental bronchi. As ventilation was increased, the temperature along the airways progressively decreased, and at a VE of 100+ 1/min the temperature at the above two sites fell to 29.2 +/- 0.5 and 33.9 +/- 0.8 degrees C, respectively. Interval points were intermediate between these extremes. With cold air, the changes were considerably more profound. During quiet breathing, local temperatures approximated those recorded in the maximum VE room-air trial, and at maximum VE, the temperatures in the proximal and distal airways were 20.5 +/- 0.6 and 31.6 +/- 1.2 degrees C, respectively. During expiration, the temperature along the airways progressively decreased as the air flowed from the periphery of the lung to the mouth: the more the cooling during inspiration, the lower the temperature during expiration. These data demonstrate that in the course of conditioning inspired air the intrathoracic and intrapulmonic airways undergo profound thermal changes that extend well into the periphery of the lung.

Adult↗
PubMed1985

Radiographic visualization of airway wall movement during oscillatory flow in dogs.

It has been suggested that radial movement of the central airway walls during oscillatory flow might contribute to the increased frequency dependence of compliance seen in chronic obstructive pulmonary disease (COPD) (J. Appl. Physiol. 26: 670-677, 1969). Radial airway wall motion has also been invoked to explain the frequency-dependent decreases in the efficiency of gas exchange during low-volume high-frequency ventilation (HFV) in histamine-bronchoconstricted dogs and in patients with respiratory insufficiency. To test the possibility that airway wall motion increases with bronchoconstriction, we measured central airway diameters using cinebronchoradiography in anesthetized tracheostomized dogs during oscillatory HFV [50 and 100 ml tidal volume (VT) at frequencies (f) of 2, 6, and 12 Hz], under control conditions, during electrical stimulation of the vagi, and after exposure to histamine aerosol. Cineradiobronchograms from two dogs were evaluated quantitatively for tracheal diameter and for lengths and diameters of a number of major airways. Under control conditions, the diameter of the airways fluctuated 7-9% of the mean with VT of 50 ml and 9-18% with VT of 100 ml in the range of frequencies studied. Bronchoconstriction produced by aerosolized histamine increased radial airway wall movement to 10-47% with VT of 50 ml, and during vagal stimulation diameters changed 7-20% at VT of 50 ml. After histamine, the central airways displayed large diameter changes during HFV, whereas more peripheral airways were markedly constricted and did not change in diameter.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗