Biomedical subjects

J H Bates

Publications and source records attributed to J H Bates.

At least 91 records · Page 5Linked to original sources

PubMed1995

Respiratory mechanics and gas exchange in postobstructive pulmonary vasculopathy.

Chronic unilateral pulmonary artery ligation induces formation of new bronchial collateral vessels in the affected lung. These vessels form precapillary anastomoses with the pulmonary circulation and the lung is perfused with arterial blood. Inspired gas is diverted to the contralateral lung to maintain the ventilation/perfusion ratio (VA/Q) and gas exchange. This study was designed to determine the mechanism responsible for this shift of ventilation, which has not previously been investigated. We studied six dogs, before and 6 months after ligation of the left main pulmonary artery. We measured pulmonary resistance (RL) and elastance (EL), minute ventilation (VE), O2 consumption (VO2) and CO2 production (VCO2) of the right and left lungs. We also examined the effect of CO2, atropine and isoproterenol on RL and EL. In the lung with ligated pulmonary artery: 1) VE was significantly reduced; 2) RL and EL were increased and were unresponsive to CO2, atropine and isoproterenol; and 3) VO2 decreased more than VCO2 and, consequently, respiratory quotient (RQ) was greater than 1. We conclude that, with chronic pulmonary artery obstruction, ventilation shifts to the contralateral lung because of an increase in RL and EL not related to airway smooth muscle tone.

Animals↗

PubMed1994

Mechanical behaviour of the canine respiratory system at very low lung volumes.

We studied the changes in dynamic elastance and resistance of the respiratory system in 6 supine, anaesthetized, paralysed, tracheostomised and open chested dogs. Tracheal pressure (Ptr), tracheal flow (V) and 3 alveolar pressures (Palv by alveolar capsule) were measured continuously for 20 min at 5 levels of positive end expiratory pressure (PEEP) between 0.1 and 0.5 kPa. The lungs were inflated to total lung capacity (TLC) at the start of each recording period. Lung elastance (EL) and resistance (RL) were estimated by fitting the equation Ptr = RLV + ELV + K to the measured data for each breath by multiple linear regression (V = volume, K = constant). Airway resistance (Raw) was obtained from the difference between Ptr and Palv. EL increased progressively in the 20 min following lung inflations. The increase in EL over this time was about 45% of its baseline value at a PEEP of 0.1 kPa compared to an increase of only about 10% at a PEEP of 0.5 kPa. In contrast, RL changed very little over the recording period at all levels of PEEP. At low levels of PEEP Palv often bore no resemblance to Ptr indicating that significant airway obstruction or closure had occurred. These results suggest that the increase in EL at low PEEP was primarily due to the accretion of airspace closure, and that nonlinear tissue mechanical properties were responsible for the lack of change in RL.

Airway Resistance↗

PubMed1994

Stability of DNA fingerprint pattern produced with IS6110 in strains of Mycobacterium tuberculosis.

To assess the stability of IS6110 restriction fragment length polymorphism patterns, DNA fingerprints of 6 Mycobacterium bovis isolates from 1 patient and of 41 Mycobacterium tuberculosis isolates from 18 patients were compared. The fingerprint pattern for a given patient remained identical or nearly identical despite recovery of the isolates during intervals which ranged from 8 months to 4.5 years. Changes in drug resistance profile did not alter a strain's fingerprint pattern.

DNA Fingerprinting↗

PubMed1994

Breathing patterns in infants and children under halothane anesthesia: effect of dose and CO2.

We studied the amplitude, timing, and shape of the airflow waveform at the mouth of spontaneously breathing children under two sets of conditions: 1) in 30 children aged 9 wk-4.5 yr at 2, 1, and 0% inspired halothane concentration and 2) in 22 children aged 5 mo-7 yr during hyperoxic CO2 rebreathing while recovering from anesthesia. Compared with control values, the relative changes in breath parameters at 1 and 2% halothane were, respectively, as follows: total cycle time -19 and -31%, tidal volume (VT) -30 and -44%, minute ventilation -11 and -17%, and VT/inspiratory time (TI) -16 and -20%. Parameters of timing and breath shape did not change except for the significant but small increase in TI/total cycle time (by 6 and 8%, respectively). With CO2 rebreathing, parameters reflecting inspiratory drive increased significantly in all patients as shown by the slopes of the regressions of these parameters against end-tidal PCO2. Mean slopes expressed in %control value per millimeter of mercury CO2 were 12.1 for minute ventilation, 8.3 for VT, and 10.67 for VT/TI. Parameters reflecting the timing and breath shape remained essentially unchanged. Our results suggest that, in children under halothane anesthesia, the amplitude, timing, and shape of the breathing pattern are controlled independently. In particular, the amplitude and timing of the breath may vary widely without any significant change in the shape.

Airway Resistance↗

PubMed1994

Temporal dynamics of pulmonary response to intravenous histamine in dogs: effects of dose and lung volume.

We measured tracheal pressure (Ptr) and tracheal flow (V) in open-chest anesthetized paralyzed dogs. The lungs were maintained at a fixed volume (initial positive end-expiratory pressure 0.5 kPa) for 80 s while small-amplitude oscillations in V at 1 and 6 Hz were applied simultaneously at the tracheal opening. A bolus of histamine was given intravenously at the start of the oscillation period. The time course of lung elastic recoil pressure (Pel) was obtained by passing a running average over Ptr to smooth out its oscillations. The oscillations themselves were separated into their 1- and 6-Hz components, as were those in V. By fitting models to the 1- and 6-Hz components of Ptr and V by recursive least squares, we obtained time courses of lung resistance at 6 Hz (RL6), dynamic lung elastance at 1 Hz (EL1), and the difference between dynamic lung resistance at 1 and 6 Hz (RL1-RL6). In four dogs we studied the effects of histamine doses of 0.05, 1.0, and 20 mg. We found that Pel increased quickly and plateaued, RL6 continued to increase throughout the oscillation period, and EL1 exhibited features of both Pel and RL6. Furthermore, the ratio of RL1-RL6 to EL1 was qualitatively similar in time course to Pel. We explain these varied time courses in terms of the development of regional ventilation inhomogeneity throughout the lung as the reaction to histamine develops. In four dogs we also studied the effects of reducing the initial positive end-expiratory pressure by 0.25 kPa and found that the changes in RL6, EL1, and RL1-RL6 were greatly magnified, presumably because of the reduced forces of parenchymal interdependence.

Airway Resistance↗

PubMed1994

Oscillatory pressure-flow relationships of canine airways: a steady-state model for different gases.

We measured the airway pressure drop (delta Paw) between the trachea and the alveolus in three normal anesthetized paralyzed dogs, together with flow (V) at the trachea. Alveolar pressure was measured using a closed-chest modification of the standard alveolar capsule technique. Measurements were made during a period of sinusoidal ventilation at 0.83 Hz with a tidal volume of 35 ml/kg, after a 30-s period of apnea. We found that the amplitude of the swings in delta Paw decreased transiently after onset of sinusoidal ventilation. We established that this decrease was due to a reflex bronchodilatation by making additional measurements on vagotomized dogs. We developed a mathematical model to account for the steady-state data that included both laminar and turbulent flow, airway wall elastance, airway gas inertance, and the Bernoulli effect at the site of tracheal pressure measurement. The model accurately described the data obtained from each dog with four different gas mixtures containing air, helium, neon, and sulfur hexafluoride. We also constructed Moody plots from the measured delta Paw-V relationships, after removing the estimated contributions of gas inertance and the Bernoulli effect from delta Paw, and found evidence of the effects of changing airway dimensions throughout a breath, V unsteadiness, and differences between inspiratory and expiratory resistances.

Airway Resistance↗

PubMed1994

Assessment of acute pleural effusion in dogs by computed tomography.

We used computed tomography (CT) to examine the effects of infusing 60 ml/kg of saline into the pleural space of four anesthetized paralyzed dogs ventilated with a constant tidal volume at a positive end-expiratory pressure of 0.5 kPa. The dogs were positioned supine, and the thoracic cavity was scanned from apex to base before and immediately after effusate loading. Each CT image was analyzed semi-automatically on a 486 personal computer with custom-designed software. We found that, despite right-side infusion, the effusate was distributed bilaterally no doubt because of the incomplete canine mediastinum. In general, the volume change of the lung was one-third and that of the chest wall was two-thirds that of the total volume infused. Most of the lung volume was contained in the caudal one-third of the lung pre-effusion, and most of the lung volume loss due to effusion was from this same region. Chest wall volume increased and in a more uniform manner post-effusion. The decrease in lung volume resulted in an increase in the mean density of the lung and an increase in its vertical density gradient as the lung was lifted upward toward the sternum by the effusate. The lung lost vertical height while the chest wall increased both its vertical and lateral dimensions after effusate loading. These results suggest that expansion of the chest wall helps preserve lung volume in the presence of acute pleural effusion. We have also demonstrated that CT is a useful tool for assessing changes in volume, shape, and density of the respiratory system.

Animals↗

PubMed1994

Serial distribution of airway mechanical properties in dogs: effects of histamine.

We measured respiratory input impedance (Zin; 8-2,048 Hz) in five dogs (anesthetized, tracheostomized, vagotomized, and mechanically ventilated) during 80 s of apnea after a bolus intravenous injection of saline or histamine (5.0 mg). In the control case, three antiresonances in Zin were found in four of the dogs, whereas in the remaining dog only two were found. The magnitude and frequency of these antiresonances were significantly altered after bronchoconstriction. To interpret Zin, a model incorporating detailed airway geometry, asymmetrical branching, and nonrigid airway walls was developed. The model fit both the saline and histamine Zin data well and predicted a serial distribution of bronchoconstriction consistent with known effects of histamine; i.e., the diameters of the most peripheral airways were reduced (26% of their control values), whereas tracheal diameters were not significantly affected. The model provided estimates of tracheal diameters that were well correlated (r = 0.92) with direct measurements. Control estimates of soft tissue viscosity (1.63 +/- 0.42 cmH2O.s) and Young's modulus (406 +/- 125 cmH2O) compared closely with values in the literature. These results indicate that bronchoconstriction induced by histamine results in significant changes in Zin over this frequency range and that by using this data analysis approach definitive physiological parameters relative to airway geometry and wall mechanical properties can be obtained from measurements made at the airway opening.

Airway Resistance↗

PubMed1994

Acute pulmonary response to intravenous histamine using forced oscillations through alveolar capsules in dogs.

We measured the time course of alveolar input impedance using two alveolar capsule oscillators after intravenous bolus administration of 20 mg of histamine in open-chest dogs. Impedances (24-200 Hz) were obtained every 2 s after an injection for 100 s. Each impedance was fit with a model consisting of a pathway (with resistance and inertance) leading from the alveolar capsule into a subpleural region (with elastance EA) that, in turn, was connected to the lung compartment (consisting of the remainder of the lung and positive end expiratory pressure system) via another pathway (with resistance RA). In all cases (6 dogs, 2 capsules each), the resistance and inertance leading from the alveolar capsules were negligible. The correlation of the relative increases in RA obtained from the two capsule oscillators in each dog was not significant. The correlation for EA also was not significant. The times at which RA achieved values of 20% greater than baseline were not significantly correlated between the two capsules, as was the case for EA. However, the baseline values of EA and RA from a given capsule were significantly correlated, as were their fractional increases with histamine. These results show that both the magnitude and timing of changes in local lung resistance and elastance are spatially extremely heterogeneous.

Airway Resistance↗

PubMed1994

Altered mechanical properties of lung parenchyma in postobstructive pulmonary vasculopathy.

Postobstructive pulmonary vasculopathy (POPV) produced by chronic unilateral ligation of one pulmonary artery, results in perfusion of the pulmonary capillaries with systemic arterial blood. As a consequence, gas exchange occurs primarily in the contralateral nonligated lung. To determine whether the mechanical properties of the lung parenchyma are changed in POPV, we compared five dogs with chronic ligation of the left main pulmonary artery with five control dogs. Separate measurements of left and right lung airway flows, tracheal pressures, and alveolar pressures were made during mechanical ventilation at frequencies between 5 and 40 breaths/min. We calculated pulmonary elastance (EL) and pulmonary (RL), airway (Raw), and tissue (Rti) resistances. At all frequencies, dogs with POPV had higher left (ligated) EL and Rti and lower right (normal) lung Rti but similar EL compared with the respective lungs from control animals. Raw was the same in both lungs. Histology showed visceral pleura thickening and encroachment of new bronchial collaterals and lymphatics on the parenchyma of the ligated lungs. The contralateral lungs were entirely normal. We conclude that in POPV 1) there is an increase, in the ligated lung, of both EL and RL, the latter likely due to histological changes of the lung parenchyma, and 2) there is a reduction of Rti in the contralateral lung.

Airway Resistance↗

PubMed1993

Regional lung impedance from forced oscillations through alveolar capsules.

We developed a technique for applying forced oscillations in flow between 5 and 200 Hz to the lung through an alveolar capsule. This provided measures of the complex alveolar input impedance of the lung, which we modelled in terms of an elastic alveolar unit connected to the rest of the lung by a peripheral airway. The estimated elastance of the alveolar compartment in 6 normal dogs was about 5 orders of magnitude greater than the elastance of the entire lung. The resistance of the airway leading into the compartment from the rest of the lung was about 5 orders of magnitude greater than the resistance of the entire airway tree. The capsule oscillation technique thus gives mechanical information about an extremely small region of the lung (in the order of 10 mm3 in volume) just under the capsule. A bolus i.v. injection of methacholine caused a variable response in the alveolar regions studied, with some regional elastances and resistances increasing while others decreased, despite the fact that overall lung resistance and elastance always increased. We conclude that our capsule oscillator technique yields precise mechanical information about very small distal regions of the lung, and that these regions respond heterogeneously to injected methacholine.

Airway Resistance↗

PubMed1993

The history of tuberculosis as a global epidemic.

TB should be thought of as a slowly progressing worldwide epidemic. Initially it was a disease of lower mammals, and the etiologic agent probably preceded the development of man on earth. It became an uncommon endemic disease in man about the time man began to settle in villages and develop agriculture. Crowding in European cities, and later the industrial revolution in Europe, provided the necessary environmental conditions for the endemic disease to become epidemic. For the next 400 years, the disease was spread by European empire-building and colonization. It came late to sub-Saharan Africa and to the Pacific Islands, and still later to the highlands of New Guinea. The epidemic gradually wanes within a large population group as resistant individuals survive and reproduce. This natural resistance is reflected in the ability of the macrophage to control intracellular growth of the organism. The resistant host shows a chronic infection primarily affecting the lungs, whereas the highly susceptible host shows a rapidly fatal illness with generalized spread of disease to many organs. Survivors of the initial infection then show another type of resistance to reinfection that is based on sensitized T cells. When this system is only partially successful, the host becomes infectious and capable of spreading the infection widely. The study of the epidemiology of TB and the evaluation of various public health measures to prevent or contain the disease requires that the investigator have an understanding of the nature and duration of the TB epidemic in the particular population under study. This factor is a much greater determinant of the course of an epidemic than any public health measure that man can institute, just as the currents in a river can have a more powerful effect on the course of a canoe than the most vigorous paddler.

Disease Outbreaks↗

PubMed1993

Acute pulmonary response to intravenous histamine at fixed lung volume in dogs.

We measured tracheal pressure (Ptr), tracheal flow, and two alveolar pressures in five open-chest anesthetized and paralyzed dogs. The lungs were maintained at a fixed volume for 50 s while small amplitude oscillations in flow at 6 Hz were applied at the tracheal opening. The measurements of alveolar pressure showed that the resulting oscillations in Ptr were virtually entirely determined by airway resistance (Raw) and consequently gave accurate estimates of the same. A 20-mg bolus of histamine was given intravenously at the start of this period when Ptr was 0.5 kPa. After approximately 10 s the mean Ptr increased sharply by approximately 40% and plateaued after approximately 25 s. Raw, in contrast, continued to increase throughout the oscillation period. Furthermore, the increases in mean Ptr were virtually identical in all dogs, whereas the increases in Raw were highly variable among the dogs. Our results suggest that the increases in mean Ptr caused by histamine were due to contraction of distal elements in the lung, whereas the changes in Raw were due mainly to constriction of more central airways.

Air Pressure↗

PubMed1993

Effect of methacholine on low-frequency mechanics of canine airways and lung tissue.

We measured tracheal flow, tracheal pressure, and alveolar capsule pressure in four anesthetized paralyzed tracheostomized open-chest dogs. Lung impedance between 0.12 and 4.88 Hz was measured with a forced volume oscillation technique before and after the intravenous administration of methacholine (MCh). Before MCh administration, lung impedance was well described by a model featuring a single airway leading to an alveolar region surrounded by tissue with a continuous distribution of viscoelastic time constants as used by Hantos et al. (J. Appl. Physiol. 68: 849-860, 1990). After MCh, however, this model gave a poor fit to the impedances. The impedances were well accounted for, however, when the model was enhanced to include an extra time constant term, which we suspect is required to account for the uneven ventilation distribution produced by MCh. Airway impedance before MCh administration was well described by a simple resistance-inertance model, but a model incorporating serial inhomogeneity of ventilation was again required after MCh. Our results support those of previous studies indicating that the impedance of the normal dog lung is well described by a homogeneously ventilated viscoelastic tissue model. In contrast, our results after MCh administration show strong evidence of marked regional ventilation inhomogeneity in addition to the rheological properties of the tissues.

Airway Resistance↗

PubMed1993

Airway and tissue impedances of canine lungs after step volume changes.

We investigated the changes in pulmonary mechanics in five anesthetized paralyzed tracheostomized open-chest dogs after step changes in lung volume. We applied small-amplitude (10-ml) volume oscillations at 6 Hz at the tracheal opening for 50-s periods, during which we applied a step volume change of 250, 500, or 750 ml to the lungs. Alveolar capsule measurements of alveolar pressure allowed us to calculate cycle-by-cycle values for airway resistance (Raw) and reactance (Xaw) and lung tissue resistance (Rti) and reactance (Xti). Before the step changes in lung volume, when transpulmonary pressure (Ptp) had a mean value of 0.65 kPa, Raw was markedly greater than Rti. The situation was reversed after the step changes, however, when Raw decreased and Rti increased. Both Raw and Xaw showed negative dependences on Ptp and hence on airway caliber, as expected, and also decreased transiently after the step volume changes, almost certainly due to a vagally mediated bronchodilation reflex. Both Rti and Xti showed clear linear dependences on Ptp and were themselves tightly coupled. Furthermore, our estimate of bulk modulus for lung tissue at 6 Hz is comparable to its previously reported values at much lower oscillation frequencies.

Airway Resistance↗

PubMed1993

Stochastic model of the pulmonary airway tree and its implications for bronchial responsiveness.

The resistance of the pulmonary conducting airway tree (Raw) is a consequence of the resistances of its component airways and how they are connected together. To date, theoretical calculations of Raw have been performed with the aid of mathematical models of the airway tree that are purely deterministic. That is, the mechanical properties of the component airways in these models are precisely defined functions of generation number. Such models take no account of the fact that the airways of a given generation are not all exactly the same but rather exhibit a spectrum of wall thicknesses, amounts of smooth muscle, and number of parenchymal attachments. In the present study, the properties of a 10-generation stochastic airway tree model are investigated. The lengths and radii of the airways in the tree are drawn randomly from probability distribution functions (PDFs), the means of which are deterministic functions of generation number and the standard deviations are assigned various values. Monte Carlo simulation is used to estimate the PDF of Raw itself in various conditions. We show that the relative width of the PDF of Raw may be comparable to that of the PDFs from which the individual airway radii were drawn. It is also shown that when bronchoconstriction is simulated by narrowing each airway by a random amount the resulting PDF for Raw may increase in width many times. We conclude that the variations in airway responsiveness seen in nature can only be properly understood when the distribution of airway properties within the lung are taken into account.

Airway Resistance↗

PubMed1993

Effect of pleural effusion on respiratory mechanics, and the influence of deep inflation, in dogs.

We wished to study how pleural effusion affects dynamic mechanics of the lung and the chest wall. We also determined if these changes could be reversed by deep lung inflations. Pleural effusion was produced by saline infusion into the pleural space. During the infusion and over the following 2 hours, dynamic elastance and resistance of the lungs, the chest wall and the whole respiratory system were recorded. Dynamic elastance and resistance of the lung increased significantly during fluid loading and were partially, and only transiently, reversed by deep inflations. Dynamic elastance and resistance of the chest wall were little affected by these procedures. Thus, pleural effusion can have significant effects on dynamic elastance and resistance of the respiratory system (ERS, RRS). The transient nature of the change in lung parameters after deep inflation suggests that therapies based on periodic lung inflations may be of little benefit to patients with this condition.

Animals↗

PubMed1993

Understanding lung tissue mechanics in terms of mathematical models.

The mechanical properties of lung tissue are important determinants of the overall mechanical behaviour of the lung itself. Our understanding of lung tissue mechanics is embodied in various mathematical models, that relate measurements of transpulmonary pressure to lung volume and flow. The purpose of this paper is to review the most basic and important of these models. Firstly, the single-compartment linear model of lung tissue is invoked to explain measurements of transpulmonary pressure and volume under quasi-static conditions, when volume excursions are modest. The exponential nonlinear extension of this model may be used to account for measurements made when volume approaches total lung capacity. Secondly, the Kelvin body as a model of the viscoelastic properties of lung tissue is considered, as a means for accounting for tissue stress adaptation and the frequency dependencies of tissue resistance and elastance. The Prandtl body is also invoked to explain tissue plastoelasticity, manifest in quasi-static hysteresis between transpulmonary pressure and volume. Finally, some more complicated and intricate extensions of these models are considered.

Humans↗