THE EFFECT OF LUNG VOLUME AND MEDIASTINAL STRUCTURES ON TRACHEAL COLLAPSIBILITY FOR IN SITU DOGS

Respiration ◽  
1981 ◽  
pp. 631-638
Author(s):  
T. Takishima ◽  
M. Nakamura ◽  
H. Sasaki
Keyword(s):  
Lung Volume

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.

In situ forming chitosan-based hydrogel as a lung sealant for biological lung volume reduction

2015 ◽  
Vol 60 (2) ◽  
pp. 235-240 ◽  
Author(s):  
Titima Songkroh ◽  
Hongguo Xie ◽  
Weiting Yu ◽  
Guojun Lv ◽  
Xiudong Liu ◽  
...  
Keyword(s):  
Lung Volume ◽  
Volume Reduction ◽  
Lung Volume Reduction ◽  
In Situ Forming

Comparison of postnatal lung growth and development between C3H/HeJ and C57BL/6J mice

2006 ◽  
Vol 100 (5) ◽  
pp. 1577-1583 ◽  
Author(s):  
Shawn E. Soutiere ◽  
Wayne Mitzner
Keyword(s):  
Lung Volume ◽  
Lung Development ◽  
Inbred Mice ◽  
Left Lung ◽  
Transpulmonary Pressure ◽  
Mean Linear Intercept ◽  
Old Mice

Previous work by our group has demonstrated substantial differences in lung volume and morphometric parameters between inbred mice. Specifically, adult C3H/HeJ (C3) have a 50% larger lung volume and 30% greater mean linear intercept than C57BL/6J (B6) mice. Although much of lung development occurs postnatally in rodents, it is uncertain at what age the differences between these strains become manifest. In this study, we performed quasi-static pressure-volume curves and morphometric analysis on neonatal mice. Lungs from anesthetized mice were degassed in vivo using absorption of 100% O2. Pressure-volume curves were then recorded in situ. The lungs were then fixed by instillation of Zenker’s solution at a constant transpulmonary pressure. The left lung from each animal was used for morphometric determination of mean air space chord length ( Lma). We found that the lung volume of C3 mice was substantially greater than that of B6 mice at all ages. In contrast, there was no difference in Lma (62.7 μm in C3 and 58.5 μm in B6) of 3-day-old mice. With increasing age (8 days), there was a progressive decrease in the Lma of both strains, with the magnitude of the decrease in B6 Lma mice exceeding that of C3. C3 lung volume remained 50% larger. The combination of parenchymal architectural similarity with lung air volume differences and different rates of alveolar septation support the hypothesis that lung volume and alveolar dimensions are independently regulated.

In-situ pulmonary vascular morphology and lung volume in the fetal and neonatal rat

1993 ◽  
Vol 34 (3) ◽  
pp. 191-198 ◽  
Author(s):  
Kazuo Momma ◽  
Tadahiko Ito ◽  
Yoshiki Mori ◽  
Masato Yokozawa
Keyword(s):  
Lung Volume ◽  
Neonatal Rat ◽  
Vascular Morphology

Effects of body position and lung volume on in situ operating length of canine diaphragm

1990 ◽  
Vol 69 (5) ◽  
pp. 1702-1708 ◽  
Author(s):  
S. S. Margulies ◽  
G. A. Farkas ◽  
J. R. Rodarte
Keyword(s):  
Lung Volume ◽  
Body Position ◽  
Vertical Gradient ◽  
Postoperative Recovery ◽  
Optimal Force ◽  
Residual Capacity ◽  
Crural Diaphragm

The performance of the diaphragm is influenced by its in situ length relative to its optimal force-generating length (Lo). Lead markers were sutured to the abdominal surface of the diaphragm along bundles of the left ventral, middle, and dorsal regions of the costal diaphragm and the left crural diaphragm of six beagle dogs. After 2-3 wk postoperative recovery, the dogs were anesthetized, paralyzed, and scanned prone and supine in the Dynamic Spatial Reconstructor (DSR) at a total lung capacity (TLC), functional residual capacity (FRC), and residual volume (RV). The location of each marker was digitized from the reconstructed DSR images, and in situ lengths were determined. After an overdose of anesthetic had been administered to the dogs, each marked diaphragm bundle was removed, mounted in a 37 degrees C in vitro chamber, and adjusted to Lo (maximum tetanic force). The operating length of the diaphragm, or in situ length expressed as percent Lo, varied from region to region at the lung volumes studied; variability was least at RV and increased with increasing lung volume. At FRC, all regions of the diaphragm was shorter in the prone posture compared with the supine, but there was no clear gravity-dependent vertical gradient of in situ length in either posture. Because in vitro length-tension characteristics were similar for all diaphragm regions, regional in vivo length differences indicate that the diaphragm's potential to generate maximal force is nonuniform.

scholarly journals On defining total lung capacity in the mouse

2004 ◽  
Vol 96 (5) ◽  
pp. 1658-1664 ◽  
Author(s):  
Shawn E. Soutiere ◽  
Wayne Mitzner
Keyword(s):  
Lung Volume ◽  
High Pressures ◽  
Total Lung Capacity ◽  
Lung Damage ◽  
Mouse Lung ◽  
Inflation Pressure ◽  
Maximal Volume ◽  
Lung Capacity

Maximal lung volume or total lung capacity in experimental animals is dependent on the pressure to which the lungs are inflated. Although 25-30 cmH2O are nominally used for such inflations, mouse pressure-volume (P-V) curves show little flattening on inflation to those pressures. In the present study, we examined P-V relations and mean alveolar chord length in three strains (C3H/HeJ, A/J, and C57BL/6J) at multiple inflation pressures. Mice were anesthetized, and their lungs were degassed in vivo by absorption of 100% O2. P-V curves were then recorded in situ with increasing peak inflation pressure in 10-cmH2O increments up to 90 cmH2O. Lungs were quickly frozen at specific pressures for morphometric analysis. The inflation limbs never showed the appearance of a plateau, with lung volume increasing 40-60% as inflation pressure was increased from 30 to 60 cmH2O. In contrast, parallel flat deflation limbs were always observed, regardless of the inflation pressure, indicating that the presence of a flat deflation curve cannot be used to justify measurement of total lung capacity in mice. Alveolar size increased monotonically with increasing pressure in all strains, and there was no evidence of irreversible lung damage from these inflations to high pressures. These results suggest that the mouse lung never reaches a maximal volume, even up to nonphysiological pressures >80 cmH2O.

Diaphragmatic thickness-lung volume relationship in vivo

1989 ◽  
Vol 67 (4) ◽  
pp. 1560-1568 ◽  
Author(s):  
J. L. Wait ◽  
P. A. Nahormek ◽  
W. T. Yost ◽  
D. P. Rochester
Keyword(s):  
Lung Volume ◽  
In Vivo Studies ◽  
Normal Male ◽  
Diaphragm Thickness ◽  
Diaphragmatic Function ◽  
Volume Relationship ◽  
Relationship Of ◽  
The Relationship

To characterize the relationship of changes in diaphragmatic thickness during contraction to changes in lung volume, we developed a technique to measure diaphragm thickness based on M-mode ultrasonography. First, diaphragmatic thickness was measured in situ at necropsy with ultrasound and verified by measuring the same resected segment of diaphragm by ruler (correlation coefficient = 0.93, slope = 0.97). The technique of imaging the diaphragm in living subjects was developed by using a 15-MHz transducer coupled to an M-mode echocardiograph. Ten normal male volunteers were studied while sitting. The ultrasound transducer was held between the ribs in the ninth lateral interspace, and tidal volume was measured by spirometry. The thickening fraction (TF) was calculated as TF = (thickness at peak inspiration - thickness at end expiration)/thickness at end expiration for each of a series of different sized breaths. The function, TF vs. lung volume, for a range of volumes was linear for each subject and had intrasubject reproducibility with intersubject variability. We conclude that diaphragmatic TF is related to function as determined by lung volume, and this may prove to be a useful technique for in vivo studies of diaphragmatic function.

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.

Effect of tidal volume and PEEP on rate of edema formation in in situ perfused canine lobes

1988 ◽  
Vol 64 (5) ◽  
pp. 1900-1907 ◽  
Author(s):  
Z. Bshouty ◽  
J. Ali ◽  
M. Younes
Keyword(s):  
Tidal Volume ◽  
Lung Volume ◽  
Base Line ◽  
Positive End Expiratory Pressure ◽  
Edema Formation ◽  
Wide Range ◽  
Static Conditions ◽  
Cyclic Changes ◽  
Best Fit

The effects of raising tidal volume and positive end-expiratory pressure (PEEP) on rate of edema formation were studied in in situ canine left upper lobe preparations. Edema was induced by increasing blood flow to the left upper lobe (4–8 times normal). In the same animal, at equivalent flows and microvascular hydrostatic pressures, rate of edema formation observed with larger tidal volumes was significantly higher than that observed with smaller tidal volumes (0.73 +/- 0.29 vs. 0.58 +/- 0.30, P less than 0.001). Edema was also induced under static conditions (i.e., flow = 0) over a wide range of vascular pressures. Rate of edema formation was plotted against pressure and the best-fit linear regression was obtained. The slopes (g.min-1.mmHg-1.100 g-1) of the regression lines were significantly higher with larger tidal volumes compared with smaller tidal volumes [0.106 +/- 0.010 (SE) vs. 0.081 +/- 0.009, P less than 0.01]. The pressure intercepts were not different (16.1 +/- 1.6 vs. 15.7 +/- 1.8). When mean airway pressures were increased to levels equivalent to those obtained with larger tidal volumes, but by raising end-expiratory pressures, rate of edema formation dropped to levels below base line. We conclude that increasing the amplitude of cyclic changes in lung volume increases edema formation through mechanisms that are independent of changes in operating (i.e., mean) lung volume.

Effect of lung volume on the respiratory action of the canine sternomastoid

1996 ◽  
Vol 80 (3) ◽  
pp. 852-856 ◽  
Author(s):  
S. R. Muza ◽  
G. J. Criner ◽  
S. G. Kelsen
Keyword(s):  
Lung Volume ◽  
Total Lung Capacity ◽  
Mechanical Action ◽  
Cross Sectional ◽  
Rib Cage ◽  
Lung Capacity ◽  
Negative Change ◽  
Residual Capacity ◽  
Anesthetized Dogs

We tested the hypothesis that because the resting length of the canine sternomastoid (SM) muscles is relatively insensitive to lung volume change, the SM may maintain its inspiratory force generation regardless of lung volume. The relationships between SM pre- and postcontraction in situ fiber lengths and SM-produced inspiratory pressure generation [i.e., esophageal (Pes)] and rib cage displacements were examined in adult supine anesthetized dogs at residual volume (RV), functional residual capacity, and total lung capacity. SM muscle contraction was produced by isolated bilateral supramaximal electrical stimulation during hyperventilation-induced apnea. In all animals, SM contraction produced negative change in Pes (i.e., an inspiratory action). Passively increasing lung volume from RV to total lung capacity decreased (P < or = 0.01) the SM-produced Pes by -66 +/- 4% but had a relatively small effect on SM in situ pre- and postcontraction fiber length (< 3%). Whereas SM contraction at RV produced a cranial displacement of the sternum and increased the upper rib cage cross-sectional area, passively elevating lung volume diminished the SM-produced expansion of the upper rib cage. Hyperinflation did not increase the impedance of the sternum to cranial displacement during SM contraction, suggesting that hyperinflation caused a dissociation between the mechanical action of the sternum and the upper rib cage. These results suggest that mechanical dissociation of the ribs and sternum may diminish the contribution of the SM to inspiratory volume generation when breathing is done from elevated end-expiratory lung volumes.

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