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Biomedical subjects

J R Rodarte

Publications and source records attributed to J R Rodarte.

At least 91 records · Page 5Linked to original sources
PubMed1984

Regional differences in expansion in excised dog lung lobes.

The position of small metallic markers embedded within the lung parenchyma and glued to the pleural surface of four excised right caudal dog lobes were determined during stepwise deflation from an airway opening pressure of 25 cmH2O in air-filled suspended lobes and 8 cmH2O in saline-filled lobes submerged in saline. Changes in the volumes of tetrahedrons formed by four noncoplanar markers were taken as regional lung volume changes at the centroids of the tetrahedron. In both air- and saline-filled lobes at all volumes below total lobe capacity (TLC) there was considerable variability in regional volume. The variability occurred at the first step below TLC and increased with deflation. Regions behaved consistently; regions that were proportionally larger or smaller than the overall lobe at any step tended to be larger or smaller, respectively, at all steps. There was a significant correlation between the regional behavior of the air- and saline-filled lobes. The variability of regional volume did not follow any clear topographical orientation. These results indicate there is considerable variability of lung compliance within small regions. This heterogeneity of regional parenchymal properties may be the anatomical basis of the nonuniformity of regional ventilation known to occur in intact animals and excised lobes within small regions at the same vertical height.

Air↗
PubMed1983

Topographical distribution of regional lung volume in anesthetized dogs.

The distribution of regional lung volume during static deflation from total lung capacity to functional residual capacity was determined from the positions of intraparenchymal metallic markers ascertained by a biplane video roentgenographic technique in supine and prone anesthetized dogs. Regional lung volumes were linearly related to overall lung volume so that regional volume could be characterized by a ventilation index (VI), which is the ventilation per alveolus relative to the ventilation of the overall lung. For the supine position, there were vertical and cephalocaudal gradients in VI in both the upper and lower lobes. Mean VI was greater in the lower lobe than in the upper lobe, but VI was less than would be predicted from extrapolation of the upper lobe relationship. For the prone position, there was no consistent gradient in VI in any direction. The magnitude of the gradients in VI and the effects of body position suggest that, in the recumbent dog, the thoracic cavity shape is a more important determinant of regional lung volume than is the effect of gravity on the lung itself.

Anesthesia, General↗
PubMed1983

Pressure-flow relationships in a collaterally ventilating dog lung segment.

We evaluated the pressure (P)-flow (V) relationship in collaterally ventilating dog lung segments by passing He, N2, and SF6 through a bronchoscope (5 mm OD) wedged in a peripheral airway. Measurements were made at functional residual capacity (FRC) and two higher lung volumes, keeping segment-to-airway opening pressure constant (3 cmH2O) in five anesthetized, paralyzed, vagotomized, supine dogs. Average flows ranged from 5.0 to 8.0 ml/s for He, 4.5 to 7.5 ml/s for N2, and 3.4 to 4.7 ml/s for SF6. When these data were fitted as P = K1/3/3 mu V + K2 rho V2, density-dependent pressure losses were unimportant when He and N2 were used, suggesting laminar flow with these gases. A dimensionless plot of the total pressure drop relative to a reference dynamic pressure as a function of Reynolds number at the bronchoscope tip suggested that flow through the segment behaved as if it were laminar at Reynolds numbers less than 100. Furthermore, when the airway diameter used to compute the normalized pressure and Reynolds number was scaled as the cubic root of lung volume, curves for all three gases were superimposed, suggesting that the dimensions of intrasegmental/collateral airways scale as lung volume 1/3.

Animals↗
PubMed1983

Airway obstruction due to inhalation of ammonia.

Ammonia is an important chemical in industry. Accidental inhalation of ammonia has resulted in upper airway and bronchoalveolar injury, and even fatal inhalation of anhydrous ammonia has occurred. We present herein a 5-year follow-up on a patient who had no prior history of smoking or pulmonary symptoms and had overwhelming exposure to ammonia which resulted in acute respiratory failure with diffuse lung parenchymal and airway involvement. The extreme inflammation and desquamation of the mucosa of the central bronchial tree, as observed bronchoscopically, have apparently resulted in a hyperreactive bronchoconstrictive component. Because our patient had never smoked and had no history of pulmonary symptoms or wheezing, we speculate that both the central and the peripheral residual airway obstructions were a result of his inhalation injury. In addition, peripheral airway disease, suggested by the postbronchodilator flow-volume curves present during the first year of follow-up, has gradually cleared even though there is evidence of parenchymal scarring.

Accidents, Occupational↗
PubMed1982

A computational model for expiratory flow.

A mathematical model of maximal expiratory flow was developed. Coupled equations describing the pressure losses in the flow and the pressure-area behavior of the airway were integrated along the airway from the periphery to the flow-limiting site. Equations describing pressure losses in the flow were adapted from studied of bronchial casts. The bronchial anatomy utilized was that described by Weibel. Bronchial mechanical properties were obtained from measurements in excised human lungs for the central airways and by extrapolations of these data for the peripheral airways. The maximal flow for air and helium predicted by the model agrees with that of five lungs from which mechanical properties were obtained. The model predictions agree with published values of density and viscosity dependence of maximal flow. At high and midlung volumes, maximal flow is determined primarily by the wave-speed mechanism. At low lung volumes, maximal flow is primarily determined by the coupling of viscous pressure losses and airway mechanical properties.

Biomechanical Phenomena↗
PubMed1982

Stress-strain analysis and the lung.

Stress is the magnitude and direction of forces acting on a body, and strain is the magnitude and direction of deformations. Constitutive equations define the relationship between stress and strain for any material. If the material can be considered homogeneous, isotropic, and elastic--that is, if the mechanical properties are uniform and independent of direction and the deformations are reversible--the constitutive equations are greatly simplified and problems of physiological interest become more tractable. Material properties may be expressed as linear elastic constants or a strain energy function. Strain energy is most suitable for large-deformation nonlinear elasticity, but such analyses are extremely complex. Theoretically, linear elasticity is limited to very small deformations, but its applicability can be expanded by considering perturbations from an initial prestressed state, but using material properties that are functions of the initial conditions. Two independent elastic constants, the bulk modulus for volume change and the shear modulus for shape change, are required to define the material properties. For problems in which the geometry of the body and the applied forces are too complex to allow an analytic solution, the body may be broken up into many small, simple elements, and the resulting matrix of equations may be simultaneously solved by a computer. The disadvantage of this finite-element analysis, in addition to its inherent complexity, is that solutions are in terms of numbers rather than equations, and determining the effect of parameters requires that a number of sample problems be solved. Nevertheless, because of its immense power, this technique has an important place in lung mechanics.

Animals↗
PubMed1981

Frequency dependence and partitioning of respiratory impedance in dogs.

Total pulmonary resistance (Rt) and reactance (Xt) from 1 to 30 Hz were determined by time series analysis in open-chest vagotomized dogs. Rt and Xt were partitioned by retrograde catheter into central airway resistance (Rc) and reactance (Xc) and peripheral resistance (Rp) and reactance (Xp). Rt, Rc, or Rp did not change with transpulmonary pressure (Pst) from 5 to 15 cmH2O, although Rc tended to decrease and Rp to increase. Vagal stimulation (Vs) and intravenous histamine (H) increased all resistances (R) at all lung volumes (V) and produced an inverse relationship between R and V. The increases in Rt produced by H and Vs were not significantly different at any volume, but H predominantly increased Rp and Vs predominantly increased Rc. In the control (vagotomized) dogs at Pst of 5 cmH2O, Rp/Rt was 0.41 +/- 0.03 (SE). Rp/Rt was significantly increased by H but not by Vs. Control Rt decreased slightly from 5 to 10 Hz and increased from 15 to 30 Hz. The increase of Rt at higher frequencies caused by the frequency dependence of Rc was not changed by H but was augmented by Vs. The slope of Xt and Xc vs. frequency was increased by Vs but not by H. The frequency dependence of Rt and Xt above 10 Hz appears to be caused by inertial losses proximal to the 2-mm airways. Thus central and peripheral bronchoconstriction caused by Vs and H, respectively, could be differentiated by increased frequency dependence of Rt and Xt above 15 Hz.

Airway Resistance↗
PubMed1980

Viscosity and density dependence during maximal flow in man.

Maximal expiratory flow curves were obtained from ten healthy subjects white breathing air and three other gas mixtures with different densities and viscosities. From these data, the magnitudes of the dependence of maximal flow on gas density and viscosity were obtained. The scaling laws of fluid mechanics, together with a model for the flow-limiting mechanism, were used to obtain a prediction of the relationship between the density dependence and the viscosity dependence of maximal flow. Although the data for individual subjects were too variable to allow a precise comparison with this prediction, the relationship between the mean density dependence and the mean viscosity dependence of all usbjects agreed with the theoretic prediction. This agreement supports the assumption, which is frequently made, that flow resistance rather than tissue visoelasticity is the dominant contributor to peripheral resistance. Information on the relationships between the pressure drop to the flow-limiting segment and flow, gas density and viscosity, and lung volume were also obtained.

Air↗
PubMed1980

Determinants of maximal expiratory flow and density dependence in normal humans.

There is a large variability in maximal expiratory flow (V) and density dependence (DD) in normal humans. Lung mechanics and flow-volume curves were obtained in 40 normal males while they breathed air or helium-oxygen (80%-20%). Static lung recoil (Pst) at 50% vital capacity, total lung capacity, and pulmonary resistance each correlated (P < 0.05) with airflow at 50% vital capacity. The relationship of V and Pst was described by Pst = 1/2 p V2/A2 + RV, where p is gas density, A is the critical area at the flow-limiting site, and R is peripheral resistance. At constant Pst and R, this simplified equation predicts an inverse relation between DD and airflow, which was found at recoil pressures of 8 and 7 cmH2O (P < 0.05). If peripheral losses are small, subjects with smaller flow-limiting airways would have lower airflows but higher DD than subjects with larger airways. Our findings are consistent with concept of dysanaptic growth and suggest that the central airways play a significant role in determining V and DD in normal humans.

Adult↗
PubMed1980

Density dependence of maximal expiratory flow in chronic obstructive pulmonary disease.

Pulmonary mechanics were studied in 22 patients with chronic obstructive pulmonary disease (COPD) who had no evidence of asthma. Eleven of the 22 patients had a density dependence of maximal expiratory flow within the reported normal range. Patients with normal density dependence (responders) were not different from those with decreased density dependence (nonresponders) in mean age, smoking history, symptoms of cough or dyspnea, maximal expiratory flow at 75, 50, and 25% of the vital capacity during air breathing, total lung capacity, or static elastic lung recoil at 50% of the vital capacity. The nonresponders had smaller vital capacity values, larger ratios of residual volume to total lung capacity, higher resistance, and lower static recoil at total lung capacity. There was a correlation between diffusing capacity for CO and density dependence. There was an inverse relationship between the change in density dependence after inhalation of isoproterenol and initial density dependence. Dysanaptic lung growth and increased compliance of the central airways are potential mechanisms for normal density dependence in these patients. The prevalence of normal density dependence in these patients with established COPD raises serious questions concerning the usefulness of density dependence in the early detection of COPD. The differences in density dependence may indicate differences in pathogenesis of the airflow obstruction and hence may be of prognostic significance.

Airway Resistance↗
PubMed1979

Respiratory mechanics in recumbent dogs anesthetized with thiopental sodium.

Pressure-volume (PV) and conductance-volume (GV) curves were obtained in trained dogs awake and then anesthetized with thiopental sodium, in the prone left lateral decubitus, and supine positions. By paired analyses, induction of anesthesia had no significant effect on lung volumes, static PV curves of the lung or chest wall, or static compliance of the lung or chest wall. In addition, change of posture had little effect on these variables in either the awake or the anesthetized state. Frequently, however, individual dogs showed changes in lung PV curves after induction of anesthesia or change of posture. These PV curve shifts were not accompanied by predictable changes in GV relations. Therefore, we concluded that such changes in the lung PV curve reflect either local artifacts or local deformation of the respiratory system.

Anesthesia↗
PubMed1979

Distribution of regional volumes and ventilation in excised canine lobes.

A linear elasticity solution for the gravitational deformation of excised lungs was obtained. The accuracy of our solution was examined by comparing predicted and measured displacements of markers glued to the surface of canine lower lobes. The equations describing the strains in a lobe were used to predict the distribution of regional volumes and the slope of phase III (S3) of a single-breath oxygen (SBO2) test. The analysis predicted a negative S3. However, S3 was found to be positive in the five lobes tested, suggesting that factors other than gravity were responsible for the observed pattern of ventilation. In SBO2 tests repeated with increasing delays at end inflation, S3 progressively decreased, became negative, and was eventually abolished. Our equations predicted the most negative observed S3 well. We conclude that continuum mechanics can be used to describe the gravitational deformation of lungs and the resulting effect on ventilation distribution.

Animals↗
PubMed1979

Effect of elastase and ventilation on elastic recoil of excised dog lungs.

The effect of porcine pancreatic elastase and mechanical ventilation on tissue elastic recoil was examined in excised dog lung lobes. Lobes incubated for one hour with an elastase-buffer mixture showed a significant (P less than 0.001) left shift of the liquid-filled pressure-volume curve at all pressures measured (0 to 12 cm H2O) when compared to lobes treated with buffer only. These results suggest that the contribution of elastin to the elastic properties of lung tissue is greatest at mid-lung volumes, but that it also contributes to delimiting maximal lung volume. Elastase and buff-treated lobes were inflated cyclically with humidified air to a pressure of 20 cm H2O 6 times per min during a 16-hour period. This mechanical ventilation caused no further decrease of tissue elastic recoil. Ventilation did cause an unexpected increase in the elastic recoil of liquid-filled lobes that was significant at pressures of 4 cm H2O (P less than 0.025) or more (P less than 0.001). Elastase and buffer-treated lobes showed an almost identical rightward shift of the pressure-volume curve after ventilation when compared to the respective nonventilated control lobes. This increased recoil cannot be attributed to altered surface tension.

Animals↗