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

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.

1983 ◽  
Vol 54 (4) ◽  
pp. 1048-1056 ◽  
Author(s):  
R. D. Hubmayr ◽  
B. J. Walters ◽  
P. A. Chevalier ◽  
J. R. Rodarte ◽  
L. E. Olson

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.


1995 ◽  
Vol 78 (3) ◽  
pp. 1030-1036 ◽  
Author(s):  
J. L. Wait ◽  
D. Staworn ◽  
D. C. Poole

One of the determinants of muscular force is the number of myofibrils in parallel, which is approximated by thickness. To better understand the heterogeneity of diaphragm thickness, we quantified the interregional and radial patterns of thickness of nine canine diaphragms rapidly perfusion fixed in situ with glutaraldehyde at functional residual capacity (FRC) (n = 6) and total lung capacity (TLC) (n = 3). Thickness was determined gravimetrically from punch biopsies radiating from the central tendon to rib cage insertion in ventral, middle, and dorsal costal and crural regions. For comparison, the contralateral unfixed hemidiaphragm was sampled in the same fashion. The findings of this investigation include the following. 1) The costal diaphragm exhibits the same pattern of interregional heterogeneity at FRC, TLC, and in the freshly excised state. 2) The costal diaphragm is significantly thinner at FRC in situ (0.17 +/- 0.01 cm) than is the freshly excised contralateral diaphragm (0.21 +/- 0.01 cm; P < 0.05), whereas there is no significant difference between thickness at TLC and the freshly excised state. 3) There is significant, previously underscribed, radial tapering from the rib cage attachment (0.24 +/- 0.02) to the central tendon insertion (0.15 +/- 0.01 cm; P < 0.05) that is exaggerated at TLC. 4) With passive inflation from FRC to TLC, the greatest increase in thickness occurs close to the rib cage attachment for the ventral and medial costal regions but close to the central tendon in the dorsal and crural regions. We conclude that the diaphragm at FRC and TLC exhibits radial thickness heterogeneity that cannot be predicted from dimensions of the freshly excised diaphragm.(ABSTRACT TRUNCATED AT 250 WORDS)


1991 ◽  
Vol 70 (4) ◽  
pp. 1554-1562 ◽  
Author(s):  
J. D. Road ◽  
A. M. Leevers ◽  
E. Goldman ◽  
A. Grassino

Active expiration is produced by the abdominal muscles and the rib cage expiratory muscles. We hypothesized that the relative contribution of these two groups to expiration would affect diaphragmatic length and, hence, influence the subsequent inspiration. To address this question we measured the respiratory muscle response to expiratory threshold loading in spontaneously breathing anesthetized dogs. Prevagotomy, the increase in lung volume (functional residual capacity) and decrease in initial resting length of the diaphragm were attenuated by greater than 50% of values predicted by the passive relationships. Diaphragmatic activation (electromyogram) increased and tidal volume (VT) was preserved. Postvagotomy, effective expiratory muscle recruitment was abolished. The triangularis sterni muscle remained active, and the increase in lung volume was attenuated by less than 15% of that predicted by the passive relationship. Diaphragmatic length was shorter than predicted. VT was not restored, even though costal diaphragmatic and parasternal intercostal electromyogram increased. During expiratory threshold loading with abdominal muscles resected and vagus intact, recruitment of the rib cage expiratory muscles produced a reduction in lung volume comparable with prevagotomy; however, diaphragmatic length decreased markedly. Both the rib cage and abdominal expiratory muscles may defend lung volume; however, their combined action is important to restore diaphragmatic initial length and, accordingly, to preserve VT.


1989 ◽  
Vol 67 (4) ◽  
pp. 1438-1442 ◽  
Author(s):  
G. A. Farkas ◽  
M. Estenne ◽  
A. De Troyer

A change from the supine to the head-up posture in anesthetized dogs elicits increased phasic expiratory activation of the rib cage and abdominal expiratory muscles. However, when this postural change is produced over a 4- to 5-s period, there is an initial apnea during which all the muscles are silent. In the present studies, we have taken advantage of this initial silence to determine functional residual capacity (FRC) and measure the subsequent change in end-expiratory lung volume. Eight animals were studied, and in all of them end-expiratory lung volume in the head-up posture decreased relative to FRC [329 +/- 70 (SE) ml]. Because this decrease also represents the increase in lung volume as a result of expiratory muscle relaxation at the end of the expiratory pause, it can be used to determine the expiratory muscle contribution to tidal volume (VT). The average contribution was 62 +/- 6% VT. After denervation of the rib cage expiratory muscles, the reduction in end-expiratory lung volume still amounted to 273 +/- 84 ml (49 +/- 10% VT). Thus, in head-up dogs, about two-thirds of VT result from the action of the expiratory muscles, and most of it (83%) is due to the action of the abdominal rather than the rib cage expiratory muscles.


1980 ◽  
Vol 49 (6) ◽  
pp. 946-952 ◽  
Author(s):  
C. A. Bradley ◽  
N. R. Anthonisen

The effects of a variety of restrictive procedures on lung mechanics were studied in eight healthy subjects. Rib cage restriction decreased total lung capacity (TLC) by 43% and significantly increased elastic recoil and maximum expiratory flow (MEF). Subsequent immersion of four subjects with rib cage restriction resulted in no further change in either parameter; shifts of blood volume did not reverse recoil changes during rib cage restriction. Abdominal restriction decreased TLC by 40% and increased MEF and elastic recoil, but recoil was increased significantly less than was the case with rib cage restriction. Further, at a given recoil pressure, MEF was less during rib cage restriction than during either abdominal restriction or no restriction. Measurements of the unevenness of inspired gas distribution by the single-breath nitrogen technique showed increased unevenness during rib cage restriction, which was significantly greater than that during abdominal restriction. We conclude that lung volume restriction induces changes in lung function, but the nature of these changes depends on how the restriction is applied and therefore cannot be ascribed to low lung volume breathing per se.


1988 ◽  
Vol 64 (6) ◽  
pp. 2482-2489 ◽  
Author(s):  
P. Leblanc ◽  
E. Summers ◽  
M. D. Inman ◽  
N. L. Jones ◽  
E. J. Campbell ◽  
...  

The capacity of inspiratory muscles to generate esophageal pressure at several lung volumes from functional residual capacity (FRC) to total lung capacity (TLC) and several flow rates from zero to maximal flow was measured in five normal subjects. Static capacity was 126 +/- 14.6 cmH2O at FRC, remained unchanged between 30 and 55% TLC, and decreased to 40 +/- 6.8 cmH2O at TLC. Dynamic capacity declined by a further 5.0 +/- 0.35% from the static pressure at any given lung volume for every liter per second increase in inspiratory flow. The subjects underwent progressive incremental exercise to maximum power and achieved 1,800 +/- 45 kpm/min and maximum O2 uptake of 3,518 +/- 222 ml/min. During exercise peak esophageal pressure increased from 9.4 +/- 1.81 to 38.2 +/- 5.70 cmH2O and end-inspiratory esophageal pressure increased from 7.8 +/- 0.52 to 22.5 +/- 2.03 cmH2O from rest to maximum exercise. Because the estimated capacity available to meet these demands is critically dependent on end-inspiratory lung volume, the changes in lung volume during exercise were measured in three of the subjects using He dilution. End-expiratory volume was 52.3 +/- 2.42% TLC at rest and 38.5 +/- 0.79% TLC at maximum exercise.


1986 ◽  
Vol 60 (4) ◽  
pp. 1198-1202 ◽  
Author(s):  
F. D. McCool ◽  
B. M. Pichurko ◽  
A. S. Slutsky ◽  
M. Sarkarati ◽  
A. Rossier ◽  
...  

Previous studies suggest that abdominal binding may affect the interaction of the rib cage and the diaphragm over the tidal range of breathing in quadriplegia. To determine whether abdominal binding influences rib cage motion over the entire range of inspiratory capacity, we used spirometry and the helium-dilution technique to measure functional residual capacity (FRC), inspiratory capacity, and total lung capacity (TLC) in eight quadriplegic and five normal subjects in supine, tilted (37 degrees), and seated positions. Combined data in all three positions indicated that, with abdominal binding, FRC and TLC decreased in normal subjects [delta FRC = -0.33 + 0.151 (SD) P less than 0.01); delta TLC = -0.16 + 0.121, P less than 0.05]. In quadriplegia there was also a reduction in FRC with binding (delta FRC = -0.32 + 0.101, P less than 0.001). However, TLC increased in quadriplegia (delta TLC = 0.07 + 0.061, P less than 0.025). In an additional six quadriplegic and five normal subjects, we used magnetometers to define the influences of abdominal binding on rib cage dimensions and TLC. In quadriplegia, rib cage dimensions were increased at TLC with abdominal binding, whereas there was no change in normals. Our data suggest that this inspiratory effect of abdominal binding on augmenting rib cage volume in quadriplegia is greater than the effect of impeding diaphragm descent, and thus abdominal binding produces a net increase in TLC in quadriplegia.


1992 ◽  
Vol 73 (1) ◽  
pp. 151-159 ◽  
Author(s):  
D. C. Poole ◽  
O. Mathieu-Costello

To determine the potential range of diaphragm sarcomere lengths in situ and the effect of changes in sarcomere length on capillary and fiber geometry, rat diaphragms were perfusion fixed in situ with glutaraldehyde at different airway pressures and during electrical stimulation. The lengths of thick (1.517 +/- 0.007 microns) and thin (1.194 +/- 0.048 microns) filaments were not different from those established for rat limb muscle. Morphometric techniques were used to determine fiber cross-sectional area, sarcomere length, capillary orientation, and capillary length and surface area per fiber volume. All measurements were referenced to sarcomere length, which averaged 2.88 +/- 0.08 microns at -20 to -25 cmH2O airway pressure (residual volume) and 2.32 +/- 0.05 microns at +20 to +26 cmH2O airway pressure (total lung capacity). The contribution of capillary tortuosity and branching to total capillary length was dependent on sarcomere length and varied from 5 to 22%, consistent with that shown previously for mammalian limb muscles over this range of sarcomere lengths. Capillary length per fiber volume [Jv(c,f)] was significantly greater at residual volume (3,761 +/- 193 mm-2) than at total lung capacity (3,142 +/- 118 mm-2) and correlated with sarcomere length [l; r = 0.628, Jv(c,f) = 876l + 1,156, P less than 0.01; n = 18]. We conclude that the diaphragm is unusual in that the apparent in situ minimal sarcomere length is greater than 2.0 microns.(ABSTRACT TRUNCATED AT 250 WORDS)


1979 ◽  
Vol 46 (1) ◽  
pp. 67-73 ◽  
Author(s):  
C. R. Inners ◽  
P. B. Terry ◽  
R. J. Traystman ◽  
H. A. Menkes

The effects of changing lung volume (VL) on collateral resistance (Rcoll) and total airways resistance (Raw) were compared in six young volunteers. At functional residual capacity (FRC) = 55% total lung capacity (TLC), mean Rcoll was 4,664 +/- 1,518 (SE) cmH2O/(l/s) and mean Raw was 1.57 +/- 0.11 (SE) cmH2O/l/s). When VL increased to 80% TLC, Rcoll decreased by 63.3 +/- 7.8%, and Raw decreased by 50.3 +/- 4.2 (SE) %. The decrease in Rcoll with increasing lung volume was not statistically different from that of Raw (P less than 0.05). If the airways obstructed for measurements of Rcoll served between 2 and 5% of the lungs, then Rcoll was approximately 50 times as great as the resistance to flow through airways serving the same volume of lung at FRC. The relationship did not change significantly when VL increased by 25% TLC. If changes in Raw reflect changes in airways supplying sublobar portions of lung, these results indicate that there is no tendency for the redistribution of ventilation through airways and collateral pathways with changes in VL in young subjects.


2004 ◽  
Vol 96 (5) ◽  
pp. 1658-1664 ◽  
Author(s):  
Shawn E. Soutiere ◽  
Wayne Mitzner

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.


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