Effects of atropine on natural deflation flows and P-V curves of the isolated lung lobe

1975 ◽  
Vol 38 (1) ◽  
pp. 46-51 ◽  
Author(s):  
E. Goldman ◽  
R. J. Puy
Keyword(s):  
Lung Volume ◽  
Static Pressure ◽  
Transpulmonary Pressure ◽  
Significant Shift ◽  
Lung Lobe ◽  
Isolated Lung ◽  
Before And After ◽  
Proportionate Change ◽  
Airway Conductance ◽  
Lung Lobes

Static pressure-volume (P-V) curves and natural deflation flows (NDF) in isolated dog's lung lobes were obtained before and after atropine. Since elastic pressure was the driving force for the expiratory flow this preparation was devoid of the influence of compressive forces. A significant shift to the left of the P-V curve was observed after atropine. Mean increase in volume in the range from 30 to 2 cmH2O transpulmonary pressure (Ptp) was 0.6 ml/g (about 4% increase in percent of maximal lung volume MLV). NDF at the same Ptp (referred to as airway conductance) were significantly higher after atropine (mean increase 3 ml/s per g, about 0.15 l/s). Increase in lung volume after atropine was interpreted as evidence of relaxation of residual bronchomotor tone which in turn, by increasing airway diameters, may produce higher flows. When NDF were plotted against volume, differences between control and atropine were reduced. This was attributed to the observed leftward displacement of the P-V curve. The linear relationship found between NDF and volume in the range 2–8 cmH2O of Ptp (about 35–75% MLV) suggests a proportionate change in airway conductance with lung size. This could indicate that the lobes behaved homogeneously during passive deflation. This pattern was not modified by atropine.

Volume shifts with partial submersion of isolated lung lobes

1979 ◽  
Vol 47 (6) ◽  
pp. 1143-1147 ◽  
Author(s):  
G. T. Ford ◽  
D. Gillett ◽  
N. R. Anthonisen
Keyword(s):  
Airway Pressure ◽  
Compressive Force ◽  
Water Displacement ◽  
Lung Lobe ◽  
Isolated Lung ◽  
Tissue Movement ◽  
Volume Shift ◽  
Lung Lobes

When an isolated lung lobe is partially submerged, volume moves from the submerged part to the unsubmerged part. We partially submerged isolated dog lobes of known weight and volume, and measured airway pressure and, by water displacement, the volume of the submerged part. The lobe was then air-dried and sectioned at the waterline and each part weighed. Multiplying lobar volume by the fractional weight of the submerged part yielded the volume of the submerged part before immersion, and therefore the volume shift to the unsubmerged part due to immersion. Dividing this volume shift by the immersion-induced change in airway pressure gave the compliance (Cr') of the unsubmerged part. Cr' was compared to Cr, the compliance of the unsubmerged part when it was inflated with air. Cr/Cr' was linearly related to the degree of immersion: as immersion increased Cr/Cr' fell; so when lobes were 80% immersed Cr/Cr' was 0.3--0.5, indicating that compressing the lower part of the lung made the upper easier to expand. This behavior could be explained if with immersion lung units moved from the submerged part to the unsubmerged part and this shift increased with the degree of immersion. We demonstrated that when one part of a lobe was compressed lung units moved away from the compressive force and that this movement could occur without similar movement of the pleural surace. Tissue movement probably accounted at least in part for our results.

Effect of lung volume on collateral ventilation in the dog

1980 ◽  
Vol 49 (1) ◽  
pp. 9-15 ◽  
Author(s):  
J. Kaplan ◽  
R. C. Koehler ◽  
P. B. Terry ◽  
H. A. Menkes ◽  
R. J. Traystman
Keyword(s):  
Lung Volume ◽  
Transpulmonary Pressure ◽  
Relative Increase ◽  
Small Airways ◽  
Lung Inflation ◽  
Before And After ◽  
Collateral Pathways ◽  
Flow Through ◽  
Collateral Ventilation

We studied the effect of lung volume on resistance through collateral pathways (Rcoll) and small airways (Rsaw) before and after the injection of methacholine into obstructed segments of intact dogs. Before methacholine, Rcoll decreased 15.0 ± 4.9 (SE)% per cmH2O increase in transpulmonary pressure (Ptp) and Rsaw decreased 5.1 ± 7.0 (SE)% per cmH2O increase in Ptp. Following methacholine, lung inflation resulted in similar decreases in Rcoll and Rsaw. The fall in Rcoll was significantly greater than the fall in Rsaw. When pressure in an obstructed segment (Ps) was increased with constant Ptp (nonhomogeneous inflation), Rcoll fell approximately half as much for each cmH2O increase in pressure compared to when Ptp was increased (homogeneous inflation). We conclude 1) that increases in lung volume have small effects on Rsaw so that there is a relative increase in flow through collateral channels serving obstructed poritons of lung and 2) that Rcoll is a function of the size of the obstructed segment that increases more under homogeneous than nonhomogeneous conditions.

scholarly journals Impact of microvascular circulation on peripheral lung stability

2004 ◽  
Vol 287 (4) ◽  
pp. L879-L889 ◽  
Author(s):  
Ferenc Peták ◽  
Barna Babik ◽  
Zoltán Hantos ◽  
Denis R. Morel ◽  
Jean-Claude Pache ◽  
...  
Keyword(s):  
Lung Volume ◽  
Blood Perfusion ◽  
Transpulmonary Pressure ◽  
Basal Membrane ◽  
Pulmonary Capillaries ◽  
Alveolar Collapse ◽  
Peripheral Lung ◽  
Before And After ◽  
The Stability ◽  
The Individual

The involvement of pulmonary circulation in the mechanical properties was studied in isolated rat lungs. Pulmonary input impedance (ZL) was measured at a mean transpulmonary pressure (Ptpmean) of 2 cmH2O before and after physiological perfusion with either blood or albumin. In these lungs and in a group of unperfused lungs, ZL was also measured at Ptpmean values between 1 and 8 cmH2O. Airway resistance ( Raw) and parenchymal damping (G) and elastance (H) were estimated from ZL. End-expiratory lung volume (EELV) was measured by immersion before and after blood perfusion. The orientation of the elastin fibers relative to the basal membrane was assessed in additional unperfused and blood-perfused lungs. Pressurization of the pulmonary capillaries significantly decreased H by 31.5 ± 3.7% and 18.7 ± 2.7% for blood and albumin, respectively. Perfusion had no effect on Raw but markedly altered the Ptpmean dependences of G and H <4 cmH2O, with significantly lower values than in the unperfused lungs. At a Ptpmean of 2 cmH2O, EELV increased by 31 ± 11% ( P = 0.01) following pressurization of the capillaries, and the elastin fibers became more parallel to the basal membrane. Because the organization of elastin fibers results in smaller H values of the individual alveolus, the higher H in the unperfused lungs is probably due to a partial alveolar collapse leading to a loss in lung volume. We conclude that the physiological pressure in the pulmonary capillaries is an important mechanical factor in the maintenance of the stability of the alveolar architecture.

Effects of lung volume on airway resistance during induced constriction in papain-treated rabbits

1996 ◽  
Vol 80 (6) ◽  
pp. 1872-1879 ◽  
Author(s):  
T. Nagase ◽  
H. Matsui ◽  
E. Sudo ◽  
T. Matsuse ◽  
M. S. Ludwig ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Airway Smooth Muscle ◽  
Lung Volume ◽  
Airway Resistance ◽  
Transpulmonary Pressure ◽  
Airway Narrowing ◽  
Tissue Resistance ◽  
Before And After ◽  
Baseline Conditions ◽  
Different Levels

It has been reported that both the elasticity of the cartilage and airway-parenchymal interdependence can modify shortening of the airway smooth muscle and airway narrowing during induced constriction. We hypothesized that induced softening of the cartilage could alter airway compliance and/or the forces of mechanical interdependence, resulting in an increased degree of airway narrowing in response to a contractile stimulus. To test this hypothesis, we compared the effects of changing lung volume on airway resistance (Raw) under baseline conditions and during methacholine (MCh)-induced constriction in papain-treated (n = 6) and control rabbits (n = 6). With use of the alveolar capsule technique, Raw was directly measured under baseline conditions at different levels of end-expiratory transpulmonary pressure (Ptp = 4-12 cmH2O). Then aerosolized MCh was delivered (0.2-25 mg/ml) and measurements were performed at different levels of Ptp (4 and 12 cmH2O). From measured tracheal flow and tracheal and alveolar pressure in open-chest animals during mechanical ventilation (tidal volume = 6 ml/kg, breathing frequency = 1 Hz), we calculated Raw by subtracting tissue resistance from lung resistance. Papain treatment significantly increased Raw both under baseline conditions and after induced constriction. We found that increasing Ptp decreased Raw before and after MCh in both groups; however, the effects of changing Ptp on Raw were less in papain-treated animals. These observations suggest that both cartilage elasticity and mechanical interdependence are important determinants of airway smooth muscle shortening. The observation that volume dependence of Raw was less in papain-treated animals is consistent with the hypothesis that papain effects significant changes in the parenchymal attachments.

Pulmonary effects of acute and chronic antigen exposure of immunized guinea pigs

1979 ◽  
Vol 46 (2) ◽  
pp. 346-353 ◽  
Author(s):  
P. D. Pare ◽  
M. C. Michoud ◽  
R. C. Boucher ◽  
J. C. Hogg
Keyword(s):  
Lung Volume ◽  
Guinea Pigs ◽  
Transpulmonary Pressure ◽  
Allergic Alveolitis ◽  
Histological Lesion ◽  
Acute Group ◽  
Before And After ◽  
Residual Capacity ◽  
Group 2 ◽  
Group 1

Subdivisions of lung volume and pressure-volume (PV) curves of the lung and chest wall were measured in guinea pigs immunized to ovalbumin before and after acute (group 1) and chronic (group 2) antigen exposure. The histopathology produced in chronically exposed animals was also assessed. Animals were anesthetized with pentobarbital sodium and studied in a pressure-sensitive body plethysmograph, using a fluid-filled esophageal catheter to measure transpulmonary pressure (PL). Functional residual capacity (FRC) was determined by the Boyle's law technique; total lung capacity (TLC) was defined as the lung volume at a PL of 30 cmH20, and residual volume (RV) was defined as the lung volume at a transrespiratory pressure of -50 cmH2O. Acute antigen challenge of group 1 animals resulted in a decrease in TLC (22%), and increases in FRC (20%) and RV (110%), suggesting combined bronchoconstriction and alveolar duct constriction. Chronic antigen exposure of group 2 animals resulted in minimal changes in subdivisions of lung volume and PV curves, and produced a histological lesion resembling allergic alveolitis rather than asthma.

Effects of airway smooth muscle contraction and inflammation on lung tissue compliance

2021 ◽  
Author(s):  
Magali Boucher ◽  
Cyndi Henry ◽  
Fatemeh Khadangi ◽  
Alexis Dufour-Mailhot ◽  
Sophie Tremblay-Pitre ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Single Dose ◽  
Airway Smooth Muscle ◽  
Lung Tissue ◽  
Lung Volume ◽  
Static Pressure ◽  
Pulmonary Inflammation ◽  
Smooth Muscle Contraction ◽  
Before And After ◽  
Tissue Compliance

There are renewed interests in using the parameter K of Salazar-Knowles' equation to assess lung tissue compliance. K either decreases or increases when the lung's parenchyma stiffens or loosens, respectively. However, whether K is affected by other common features of respiratory diseases, such as inflammation and airway smooth muscle (ASM) contraction, is unknown. Herein, male C57BL/6 mice were treated intranasally with either saline or lipopolysaccharide (LPS) at 1 mg/Kg to induce pulmonary inflammation. They were then subjected to either a multiple or a single-dose challenge with methacholine to activate ASM to different degrees. A quasi-static pressure-driven partial pressure-volume maneuver was performed before and after methacholine. The Salazar-Knowles' equation was then fitted to the deflation limb of the P-V loop to obtain K, as well as the parameter A, an estimate of lung volume (inspiratory capacity). The fitted curve was also used to derive the quasi-static elastance (Est) at 5 cmH2O. The results demonstrate that LPS and both methacholine challenges increased Est. LPS also decreased A, but did not affect K. In contradistinction, methacholine decreased both A and K in the multiple-dose challenge, while it decreased K but not A in the single-dose challenge. These results suggest that LPS increases Est by reducing the open lung volume (A) and without affecting tissue compliance (K), while methacholine increases Est by decreasing tissue compliance with or without affecting lung volume. We conclude that lung tissue compliance, assessed using the parameter K of Salazar-Knowles' equation, is insensitive to inflammation but sensitive to ASM contraction.

Methacholine-induced bronchoconstriction in dogs: effects of lung volume and O3 exposure

1988 ◽  
Vol 65 (6) ◽  
pp. 2679-2686 ◽  
Author(s):  
S. T. Kariya ◽  
S. A. Shore ◽  
W. A. Skornik ◽  
K. Anderson ◽  
R. H. Ingram ◽  
...  
Keyword(s):  
Lung Volume ◽  
Maximal Response ◽  
Maximal Effect ◽  
Response Curves ◽  
Lung Volumes ◽  
Before And After ◽  
Residual Capacity ◽  
Induced Changes ◽  
Conducting Airways ◽  
Concentration Response Curve

The maximal effect induced by methacholine (MCh) aerosols on pulmonary resistance (RL), and the effects of altering lung volume and O3 exposure on these induced changes in RL, was studied in five anesthetized and paralyzed dogs. RL was measured at functional residual capacity (FRC), and lung volumes above and below FRC, after exposure to MCh aerosols generated from solutions of 0.1-300 mg MCh/ml. The relative site of response was examined by magnifying parenchymal [RL with large tidal volume (VT) at fast frequency (RLLS)] or airway effects [RL with small VT at fast frequency (RLSF)]. Measurements were performed on dogs before and after 2 h of exposure to 3 ppm O3. MCh concentration-response curves for both RLLS and RLSF were sigmoid shaped. Alterations in mean lung volume did not alter RLLS; however, RLSF was larger below FRC than at higher lung volumes. Although O3 exposure resulted in small leftward shifts of the concentration-response curve for RLLS, the airway dominated index of RL (RLSF) was not altered by O3 exposure, nor was the maximal response using either index of RL. These data suggest O3 exposure does not affect MCh responses in conducting airways; rather, it affects responses of peripheral contractile elements to MCh, without changing their maximal response.

Mechanisms leading to lung edema in pulmonary embolization

1960 ◽  
Vol 198 (3) ◽  
pp. 543-546 ◽  
Author(s):  
S. A. Kabins ◽  
J. Fridman ◽  
J. Neustadt ◽  
G. Espinosa ◽  
L. N. Katz
Keyword(s):  
Pulmonary Edema ◽  
Capillary Permeability ◽  
Lysergic Acid ◽  
Lung Edema ◽  
Pulmonary Infarction ◽  
Edema Formation ◽  
Lung Lobe ◽  
Pulmonary Embolization ◽  
Sympathetic Nervous ◽  
Lung Lobes

A localized pulmonary infarction was produced by injecting a starch suspension into the pulmonary artery wedge position of one lung lobe in pentobarbitalized dogs, and the effect of three so-called antiserotonins on the ensuing pulmonary edema was determined. Edema was inhibited in the nonembolized lung lobes in 88% of the B.A.S. (1-benzyl-2-methyl-5-methoxytryptamine HCl), 45% of the DHE (dihydroergotamine), and 12% of the BOL (2-brom- d-lysergic acid diethylamide) dogs. Reasons are given for assuming that the actions of B.A.S. and DHE are due to their antiadrenergic rather than to any antiserotonin properties which they may have. Serotonin, therefore, at most has a slight role in the pulmonary edema formation caused by starch emboli. It is postulated that the emboli by producing an infarct and setting up a reflex mediated through the sympathetic nervous system, cause the release in turn of catecholamines and of histamine, the latter being immediately responsible for the capillary permeability change leading to pulmonary edema.

Airway closure and reopening assessed by the alveolar capsule oscillation technique

1996 ◽  
Vol 80 (6) ◽  
pp. 2077-2084 ◽  
Author(s):  
D. R. Otis ◽  
F. Petak ◽  
Z. Hantos ◽  
J. J. Fredberg ◽  
R. D. Kamm
Keyword(s):  
Lung Volume ◽  
Input Impedance ◽  
Transpulmonary Pressure ◽  
Closing Volume ◽  
Airway Closure ◽  
Breathing Cycle ◽  
Abrupt Increase ◽  
Consistent Effect ◽  
Peripheral Airways

An alveolar capsule oscillation technique was used to determine 1) the lobe pressure and volume at which airways close and reopen, 2) the effect of expiration rate on closing volume and pressure, 3) the phase in the breathing cycle at which airway closure occurs, and 4) the site of airway closure. Experiments were conducted in excised dog lobes; closure was detected by an abrupt increase in the input impedance of surfacemounted alveolar capsules. Mean transpulmonary pressure (Ptp) at closure was slightly less than zero (Ptp = -2.3 cmH2O); the corresponding mean reopening pressure was Ptp = 14 cmH2O. The expiration rate varied between 1 and 20% of total lobe capacity per second and had no consistent effect on the closing volume and pressure. When lung volume was cycled up to frequencies of 0.2 Hz, closure generally occurred on expiration rather than inspiration. These observations support the conclusion that mechanical collapse, rather than meniscus formation, is the most likely mechanism producing airway closure in normal excised dog lungs. Analysis of measured acoustic impedances and reopening pressures suggests that closure occurs in the most peripheral airways. Reopening during inspiration was often observed to consist of a series of stepwise decreases in capsule impedance, indicating a sequence of opening events.

Sign in / Sign up

Export Citation Format

Share Document