Peribronchial pressure in excised dog lungs

1978 ◽  
Vol 45 (6) ◽  
pp. 858-869 ◽  
Author(s):  
H. Sasaki ◽  
F. G. Hoppin ◽  
T. Takishima
Keyword(s):  
Smooth Muscle ◽  
Lung Volume ◽  
Radial Stress ◽  
Similar Magnitude ◽  
Alveolar Pressure ◽  
Lung Inflation ◽  
Bronchial Wall ◽  
Lobar Bronchus ◽  
Intrabronchial Pressure

To characterize the stresses which determine bronchial diameter in the lung, we estimated peribronchial pressure (Px) relative to intrabronchial pressure (Pbr) and to alveolar pressure (PA) for the main lobar bronchus of excised dog lobes using the technique of Takishima et al. (J. Appl. Physiol. 38: 875--881, 1975). The recoil of the bronchial wall, Pbr---Px, when smooth muscle was relaxed varied primarily with bronchial diameter. The recoil of the parenchyma around the bronchus, Px---Pa, varied with lung volume but was also diameter-dependent and served to double approximately the effective elastance of the bronchus in situ. We estimated recoils during slow deflations from TLC with the bronchus untreated, or pharmacologically contracted or relaxed. In untreated and relaxed states, local parenchymal and bronchial recoils were of similar magnitude to overall lung recoil (i.e., Px congruent to Ppl) except at high inflating pressure (PA -- Ppl = 30 cmH2O) where they were about half as great. With contraction, bronchial and local parenchymal recoils increased to as much as twice overall lung recoil. Contracted smooth muscle exerted a radial stress of 36+/-14 cmH2O at full lung inflation but much less during stepwise deflation.

Effects of lung volume, bronchoconstriction, and cigarette smoke on morphometric airway dimensions

1988 ◽  
Vol 64 (3) ◽  
pp. 913-919 ◽  
Author(s):  
A. L. James ◽  
P. D. Pare ◽  
J. C. Hogg
Keyword(s):  
Smooth Muscle ◽  
Cigarette Smoke ◽  
Lung Volume ◽  
Muscle Tone ◽  
Cigarette Smoke Exposure ◽  
Wall Thickening ◽  
Airway Wall ◽  
Lung Inflation ◽  
Wall Area ◽  
Airway Dimensions

To examine the role of airway wall thickening in the bronchial hyperresponsiveness observed after exposure to cigarette smoke, we compared the airway dimensions of guinea pigs exposed to smoke (n = 7) or air (n = 7). After exposure the animals were anesthetized with urethan, pulmonary resistance was measured, and the lungs were removed, distended with Formalin, and fixed near functional residual capacity. The effects of lung inflation and bronchoconstriction on airway dimensions were studied separately by distending and fixing lungs with Formalin at total lung capacity (TLC) (n = 3), 50% TLC (n = 3), and 25% TLC (n = 3) or near residual volume after bronchoconstriction (n = 3). On transverse sections of extraparenchymal and intraparenchymal airways the following dimensions were measured: the internal area (Ai) and internal perimeter (Pi), defined by the epithelium, and the external area (Ae) and external perimeter (Pe), defined by the outer border of smooth muscle. Airway wall area (WA) was then calculated, WA = Ae - Ai. Ai, Pe, and Ae decreased with decreasing lung volume and after bronchoconstriction. However, WA and Pi did not change significantly with lung volume or after bronchoconstriction. After cigarette smoke exposure airway resistance was increased (P less than 0.05); however, there was no difference in WA between the smoke- and air-exposed groups when the airways were matched by Pi. We conclude that Pi and WA are constant despite changes in lung volume and smooth muscle tone and that airway hyperresponsiveness induced by cigarette smoke is not mediated by increased airway wall thickness.

Effect of lung inflation on bronchial dimensions in the dog

1962 ◽  
Vol 17 (4) ◽  
pp. 596-600 ◽  
Author(s):  
Robert Marshall
Keyword(s):  
Functional Residual Capacity ◽  
Length Change ◽  
Lung Parenchyma ◽  
Simple Relationship ◽  
Lung Inflation ◽  
Bronchial Wall ◽  
Residual Capacity ◽  
Inflation Volume ◽  
Intrabronchial Pressure

Bronchial diameters and lengths were measured from bronchograms of separate lobes of dogs' lungs. The lobes were initially completely airless, and radiographs were taken at intrabronchial pressures of 10 and 20 cm H2O at stages during inflation of the lobe. The bronchi were dissected out, made airtight, and radiographs taken at different distending pressures. In the intact lobe the increase in bronchial diameter occurred mainly at volumes below the functional residual capacity of the lobe. At greater degrees of inflation the diameters increased only slightly and in some cases were reduced. The bronchial lengths increased throughout inflation. Full inflation of the lung caused approximately a 60% increase in bronchial diameter and a 40% increase in bronchial length. Change of intrabronchial pressure from 10 to 20 cm H2O caused only 4% increase in bronchial diameters in the inflated lobe. Comparison with the same diameters in the isolated bronchus showed that the lung parenchyma exerts traction on the bronchial wall but the traction bears no simple relationship to the inflation volume. Submitted on January 18, 1962

Extra-alveolar vessel fluid filtration coefficients in excised and in situ canine lobes

1985 ◽  
Vol 59 (5) ◽  
pp. 1555-1559 ◽  
Author(s):  
R. K. Albert ◽  
W. Kirk ◽  
C. Pitts ◽  
J. Butler
Keyword(s):  
Lung Volume ◽  
Pulmonary Circulation ◽  
Alveolar Pressure ◽  
Fluid Filtration ◽  
Significant Difference ◽  
The Mean ◽  
Stop Flow ◽  
Total Circulation ◽  
Total Fluid

We continuously weighed fully distended excised or in situ canine lobes to estimate the fluid filtration coefficient (Kf) of the arterial and venous extra-alveolar vessels compared with that of the entire pulmonary circulation. Alveolar pressure was held constant at 25 cmH2O after full inflation. In the in situ lobes, the bronchial circulation was interrupted by embolization. Kf was estimated by two methods (Drake and Goldberg). Extra-alveolar vessels were isolated from alveolar vessels by embolizing enough 37- to 74-micron polystyrene beads into the lobar artery or vein to completely stop flow. In excised lobes, Kf's of the entire pulmonary circulation by the Drake and Goldberg methods were 0.122 +/- 0.041 (mean +/- SD) and 0.210 +/- 0.080 ml X min-1 X mmHg-1 X 100 g lung-1, respectively. Embolization was not found to increase the Kf's. The mean Kf's of the arterial extra-alveolar vessels were 0.068 +/- 0.014 (Drake) and 0.069 +/- 0.014 (Goldberg) (24 and 33% of the Kf's for the total pulmonary circulation). The mean Kf's of the venous extra-alveolar vessels were similar [0.046 +/- 0.020 (Drake) and 0.065 +/- 0.036 (Goldberg) or 33 and 35% of the Kf's for the total circulation]. No significant difference was found between the extra-alveolar vessel Kf's of in situ vs. excised lobes. These results suggest that when alveolar pressure, lung volume, and pulmonary vascular pressures are high, approximately one-third of the total fluid filtration comes from each of the three compartments.

Lung inflation can cause pulmonary edema in zone I of in situ dog lungs

1980 ◽  
Vol 49 (5) ◽  
pp. 815-819 ◽  
Author(s):  
R. K. Albert ◽  
S. Lakshminarayan ◽  
W. Kirk ◽  
J. Butler
Keyword(s):  
Weight Gain ◽  
Venous Pressure ◽  
Lower Lobe ◽  
Alveolar Pressure ◽  
Weight Changes ◽  
Lung Water ◽  
Lung Weight ◽  
Lung Inflation ◽  
Pulmonary Arterial

We investigated whether increases in lung water can occur due to lung inflation in zone I when alveolar vessels are collapsed. Static left lower lobe alveolar pressure, pulmonary arterial pressure, and pulmonary venous pressure were controlled in living, anesthetized, open-chested dogs. The lobe was inflated with 6% CO2 in air and suspended from a strain gauge, which allowed continual weight recording. The lung was held in zone I conditions. Arterial and venous pressures were equal at either 1 or 5 cmH2O, relative to the base of the 10- to 14-cm-high lobes. Weight changes were measured for 5 min after 5-cmH2O increments of alveolar pressure from 0 or 5 to 30 cmH2O. Lung weight gain due to edema occurred with inflation to alveolar pressures above 10 cmH2O. Greater lung distension resulted in greater rates of weight gain. Weight loss occurred on deflation. The fluid may have leaked from distended extra-alveolar vessels. This mechanism could explain the increased lung water seen with mechanical ventilation and/or positive end-expiratory pressure breathing.

Effect of lung inflation and airway muscle tone on airway diameter in vivo

1996 ◽  
Vol 80 (5) ◽  
pp. 1581-1588 ◽  
Author(s):  
R. H. Brown ◽  
W. Mitzner
Keyword(s):  
Smooth Muscle ◽  
Basement Membrane ◽  
Muscle Contraction ◽  
Lung Volume ◽  
Airway Pressure ◽  
Muscle Tone ◽  
Smooth Muscle Contraction ◽  
Lung Inflation ◽  
Highly Nonlinear

How normal airway dimensions change with lung volume is of great importance in determining flow limitation during the normal forced vital capacity maneuver as well as in the manifestation of obstructive lung disease. The literature presents a confusing picture, with some results suggesting that airway diameter increases linearly with the cube root of lung volume and others showing a highly nonlinear relation. The effect of smooth muscle contraction on lung-airway interdependence is even less well understood. Recent morphological work explicitly assumes that airway basement membrane is nondistensible, although the lung volume at which this maximal airway size is reached is unknown. With smooth muscle contraction, folding of the epithelium and basement membrane accounts for the changes in luminal area. In this study, we measured the effect of lung inflation on relaxed and contracted airway areas by using high-resolution computed tomography at different transpulmonary pressures, each held for 2 min. We found that fully relaxed airways are quite distensible up to a pressure of 5-7 cmH2O (P < 0.001), where they reach a maximal size with no further distension up to an airway pressure of 30 cmH2O (P = 0.49). Thus relaxed airways clearly do not expand isotropically with the lung. With smooth muscle tone, the airways in different animals responded differently to lung inflation, with some animals showing minimal airway dilation up to an airway pressure of 20 cmH2O and others showing airways that were more easily dilated with lung expansion. However, maximal diameter of these moderately constricted airways was not usually achieved even up to an airway pressure of 30 cmH2O. Thus a transient deep inspiration in vivo would be expected to have only a small effect on contracted airways.

Airway distensibility and volume recruitment with lung inflation in COPD

2010 ◽  
Vol 109 (4) ◽  
pp. 1019-1026 ◽  
Author(s):  
Simonetta Baldi ◽  
Raffaele Dellacà ◽  
Leonardo Govoni ◽  
Roberto Torchio ◽  
Andrea Aliverti ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Airway Smooth Muscle ◽  
Lung Volume ◽  
Muscle Tone ◽  
Forced Expiratory Volume ◽  
Chronic Obstructive ◽  
High Resolution Computed Tomography ◽  
Lung Inflation ◽  
Control Subjects ◽  
Airway Caliber

The effects of full lung inflation on respiratory conductance (Grs) and reactance (Xrs) were measured in 15 subjects with moderate to severe chronic obstructive pulmonary disease (COPD) and 11 matched healthy control subjects. Airway distensibility was estimated from the ratio of the difference of Grs between functional residual capacity and total lung capacity to the relevant changes in lung volume (ΔGrs/ΔVl) or transpulmonary pressure (ΔGrs/ΔPtp). Similar analysis was applied to Xrs to estimate lung volume recruitment (ΔXrs/ΔVl or ΔXrs/ΔPtp). The extent of emphysema in COPD subjects was estimated from the percentage of low attenuation area (LAA) at high-resolution computed tomography. At baseline, ΔGrs/ΔVl and ΔXrs/ΔVl were significantly less in COPD than control subjects, indicating less distensibility and volume recruitment in the former. In COPD, ΔGrs/ΔPtp and ΔXrs/ΔPtp were uncorrelated with LAA but correlated with 1-s forced expiratory volume and with each other. After albuterol, both ΔGrs/ΔPtp and ΔGrs/ΔVl became significantly and negatively correlated with LAA, while ΔXrs/ΔPtp and ΔXrs/ΔVl decreased significantly independently of LAA. Moreover, ΔGrs/ΔPtp and ΔXrs/ΔPtp with lung inflation were no longer correlated with each other, suggesting that airway distensibility and volume recruitment were affected differently by airway smooth muscle tone. Assuming that Grs mainly reflects airway caliber and Xrs the number of ventilated lung units, we conclude that airway smooth muscle contributes to airway stiffness and ventilation inhomogeneities in COPD subjects with prevailing bronchitis but only to the latter in those with more emphysema. We suggest that changes of airway distensibility and volume recruitment with a bronchodilator may be useful for disease phenotyping.

Effects of lung volume and alveolar surface tension on pulmonary vascular resistance

1987 ◽  
Vol 62 (4) ◽  
pp. 1622-1626 ◽  
Author(s):  
R. Y. Sun ◽  
G. F. Nieman ◽  
T. S. Hakim ◽  
H. K. Chang
Keyword(s):  
Surface Tension ◽  
Lung Volume ◽  
Pulmonary Arterial Pressure ◽  
Lower Lobe ◽  
Venous Occlusion ◽  
Alveolar Pressure ◽  
Lung Inflation ◽  
Occlusion Technique ◽  
Pulmonary Arterial ◽  
Alveolar Surface

Utilizing the arterial and venous occlusion technique, the effects of lung inflation and deflation on the resistance of alveolar and extraalveolar vessels were measured in the dog in an isolated left lower lobe preparation. The lobe was inflated and deflated slowly (45 s) at constant speed. Two volumes at equal alveolar pressure (Palv = 9.9 +/- 0.6 mmHg) and two pressures (13.8 +/- 0.8 mmHg, inflation; 4.8 +/- 0.5 mmHg, deflation) at equal volumes during inflation and deflation were studied. The total vascular pressure drop was divided into three segments: arterial (delta Pa), middle (delta Pm), and venous (delta Pv). During inflation and deflation the changes in pulmonary arterial pressure were primarily due to changes in the resistance of the alveolar vessels. At equal Palv (9.9 mmHg), delta Pm was 10.3 +/- 1.2 mmHg during deflation compared with 6.8 +/- 1.1 mmHg during inflation. At equal lung volume, delta Pm was 10.2 +/- 1.5 mmHg during inflation (Palv = 13.8 mmHg) and 5.0 +/- 0.7 mmHg during deflation (Palv = 4.8 mmHg). These measurements suggest that the alveolar pressure was transmitted more effectively to the alveolar vessels during deflation due to a lower alveolar surface tension. It was estimated that at midlung volume, the perimicrovascular pressure was 3.5–3.8 mmHg greater during deflation than during inflation.

Characteristics of lung mechanoreceptors in spotted gar, Lepisosteus oculatus

1987 ◽  
Vol 252 (6) ◽  
pp. R1066-R1072 ◽  
Author(s):  
N. J. Smatresk ◽  
S. Q. Azizi
Keyword(s):  
Lung Volume ◽  
Transpulmonary Pressure ◽  
Volume Changes ◽  
Nerve Activity ◽  
Lung Inflation ◽  
Spotted Gar ◽  
Threshold Volume ◽  
Flow Through ◽  
Lepisosteus Oculatus

Single unit and whole nerve activity were recorded in situ from pulmonary mechanoreceptors in Lepisosteus oculatus in response to step inflation and ramp or flow through ventilation of the lung with air and varying levels of CO2 in air. Slowly adapting receptors (SAR), rapidly adapting receptors (RAR), and CO2-sensitive SAR were identified. Whole nerve activity was often present when transpulmonary pressure was 0 cmH2O and increased due to recruitment and elevated discharge of already-active fibers as lung volume rose. SAR became tonically active once the lung exceeded their threshold volume and demonstrated a rate-sensitive burst of activity on inflation and a rate-sensitive inhibition of activity after deflation of the lung. RAR responded to lung inflation or deflation with a burst of activity. Six of eleven SAR were inhibited by ventilation of the lung with from 6 to 10% CO2 in air, even when lung pressure and volume were kept constant. These receptor discharge characteristics, which were similar to those found for lungfish and amphibians, may account for the reflex responses of gar to lung volume changes.

Electron Probe Analysis of Muscle

1982 ◽  
Vol 40 ◽  
pp. 398-401
Author(s):  
A. V. Somlyo ◽  
H. Shuman ◽  
A. P. Somlyo
Keyword(s):  
Skeletal Muscle ◽  
Smooth Muscle ◽  
Sarcoplasmic Reticulum ◽  
Resting State ◽  
Binding Sites ◽  
Electron Probe ◽  
Frog Skeletal Muscle ◽  
Electron Probe Analysis ◽  
Probe Analysis

Electron probe analysis of frozen dried cryosections of frog skeletal muscle, rabbit vascular smooth muscle and of isolated, hyperpermeab1 e rabbit cardiac myocytes has been used to determine the composition of the cytoplasm and organelles in the resting state as well as during contraction. The concentration of elements within the organelles reflects the permeabilities of the organelle membranes to the cytoplasmic ions as well as binding sites. The measurements of [Ca] in the sarcoplasmic reticulum (SR) and mitochondria at rest and during contraction, have direct bearing on their role as release and/or storage sites for Ca in situ.

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