On the respiratory function of the ribs

2002 ◽  
Vol 92 (4) ◽  
pp. 1642-1646 ◽  
Author(s):  
Matteo Cappello ◽  
André De Troyer

To assess the respiratory function of the ribs, we measured the changes in airway opening pressure (Pao) induced by stimulation of the parasternal and external intercostal muscles in anesthetized dogs, first before and then after the bony ribs were removed from both sides of the chest. Stimulating either set of muscles with the rib cage intact elicited a fall in Pao in all animals. After removal of the ribs, however, the fall in Pao produced by the parasternal intercostals was reduced by 60% and the fall produced by the external intercostals was eliminated. The normal outward curvature of the rib cage was also abolished in this condition, and when the curvature was restored by a small inflation, external intercostal stimulation consistently elicited a rise rather than a fall in Pao. These findings thus confirm that the ribs play a critical role in the act of breathing by converting intercostal muscle shortening into lung volume expansion. In addition, they carry the compression that is required to balance the pressure difference across the chest wall.

2004 ◽  
Vol 96 (2) ◽  
pp. 483-488 ◽  
Author(s):  
Theodore A. Wilson ◽  
Andre De Troyer

The mechanisms of respiratory action of the intercostal muscles were studied by measuring the effect of external forces (F) applied to the ribs and by modeling the effect of F exerted by the intercostal muscles. In five dogs, with the airway occluded, cranial F were applied to individual rib pairs, from the 2nd to the 11th rib pair, and the change in airway opening pressure (Pao) was measured. The ratio Pao/F increases with increasing rib number in the upper ribs (2nd to 5th) and decreases in the lower ribs (5th to 11th). These data were incorporated into a model for the geometry of the ribs and intercostal muscles, and Pao/F was calculated from the model. For interspaces 2-8, the calculated values agree reasonably well with previously measured values. From the modeling, two mechanisms of intercostal muscle action are identified. One is the well-known Hamberger mechanism, modified to account for the three-dimensional geometry of the rib cage. This mechanism depends on the slant of an intercostal muscle relative to the ribs and on the resulting difference between the moments applied to the upper and lower ribs that bound each interspace. The second is a new mechanism that depends on the difference between the values of Pao/F for the upper and lower ribs.


1986 ◽  
Vol 60 (5) ◽  
pp. 1692-1699 ◽  
Author(s):  
A. De Troyer ◽  
V. Ninane

It is traditionally considered that the difference in orientation of the muscle fibers makes the external intercostals elevate the ribs and the internal interosseous intercostals lower the ribs during breathing. This traditional view, however, has recently been challenged by the observation that the external and internal interosseous intercostals, when contracting alone in a single interspace, have a similar effect on the ribs into which they insert. This view has also been challenged by the observation that the external and internal intercostals in a given interspace often change their length in the same direction during breathing. In an attempt to clarify the respiratory function of these muscles, we studied eight supine lightly anesthetized dogs during quiet breathing and during static inspiratory efforts. In each animal electromyographic (EMG) recordings from the external and internal interosseous intercostals were obtained in all interspaces from the second to the eighth, and selective denervations were systematically performed to ensure with complete certainty the origin of the recorded EMG activities. The external intercostals were only activated in phase with inspiration, whereas the internal interosseous intercostals were only activated in phase with expiration. These phasic EMG activities, however, were generally small in magnitude, and the muscles were often silent. Indeed, activation of the externals was always confined to the upper portion of the rib cage, whereas activation of the internals was limited to the lower portion of the rib cage. Internal intercostal activation always occurred sequentially along a caudocephalic gradient. These observations are thus compatible with the traditional view of intercostal muscle action.(ABSTRACT TRUNCATED AT 250 WORDS)


1996 ◽  
Vol 80 (6) ◽  
pp. 2097-2101 ◽  
Author(s):  
A. Legrand ◽  
T. A. Wilson ◽  
A. D. Troyer

Previous theoretical studies have postulated that the potential effect of a given respiratory muscle on lung volume or pleural pressure (i.e., its respiratory effect) is proportional to the change in length of the muscle during inflation of the passive chest wall (T. A. Wilson and A. De Troyer J. Appl. Physiol. 73: 2283-2288, 1992). To test this prediction, we have studied the parasternal intercostals in 18 interspaces in 8 supine anesthetized dogs. In each interspace, we have measured the changes in length of the medial and lateral portions of the parasternal during passive inflation and we have also assessed the changes in airway opening pressure (delta Pao) generated by these portions during isolated bilateral stimulation of the internal intercostal nerve. The results showed that 1) the medial fibers shorten more than the lateral fibers during passive inflation (P < 0.001); 2) when stimulated, the medial portion generated a larger fall in Pao than the lateral portion (P < 0.001); and 3) delta Pao was closely related to change in length (r = 0.81; P < 0.001). These observations thus imply that the medial portion of the parasternal intercostals contributes much more to lung expansion during breathing than the lateral portion. These observations also suggest, in agreement with the theoretical prediction, that measurements of the changes in length of the different respiratory muscles during passive inflation can be used to predict the potential respiratory effect of these muscles and to compare their mechanical advantages.


1990 ◽  
Vol 69 (6) ◽  
pp. 2222-2226 ◽  
Author(s):  
A. F. DiMarco ◽  
J. R. Romaniuk ◽  
G. S. Supinski

The interosseous external intercostal (EI) muscles of the upper rib cage are electrically active during inspiration, but the mechanical consequence of their activation is unclear. In 16 anesthetized dogs, we simultaneously measured EI (3rd and 4th interspaces) and parasternal intercostal (PA) (3rd interspace) electromyogram and length. Muscle length was measured by sonomicrometry and expressed as a percentage of resting length (%LR). During resting breathing, each muscle was electrically active and shortened to a similar extent. Sequential EI muscle denervation (3rd and 4th interspaces) followed by PA denervation (3rd interspace) demonstrated significant reductions in the degree of inspiratory shortening for each muscle. Mean EI muscle shortening of the third and fourth interspaces decreased from -3.4 +/- 0.5 and -3.0 +/- 0.4% LR (SE) under control conditions to -0.2 +/- 0.2 and -0.8 +/- 0.3% LR, respectively, after selective denervation of each of these muscles (P less than 0.001 for each). After selective denervation of the PA muscle, its shortening decreased from -3.5 +/- 0.3 to +0.6% LR (SE) (P less than 0.001). PA muscle denervation also caused the EI muscle in the third interspace to change from inspiratory shortening of -0.2% to inspiratory lengthening of +0.2% +/- 0.2 (P less than 0.05). We conclude that during eupneic breathing 1) the EI muscles of the upper rib cage, like the PA muscles, are inspiratory agonists and actively contribute to rib cage expansion and 2) PA muscle contraction contributes to EI muscle shortening.


2003 ◽  
Vol 94 (5) ◽  
pp. 1757-1765 ◽  
Author(s):  
André De Troyer ◽  
Matteo Cappello ◽  
Nathalie Meurant ◽  
Pierre Scillia

Expansion of the lung during inspiration results from the coordinated contraction of the diaphragm and several groups of rib cage muscles, and we have previously shown that the changes in intrathoracic pressure generated by the latter are essentially additive. In the present studies, we have assessed the interaction between the right and left hemidiaphragms in anesthetized dogs by comparing the changes in airway opening pressure (ΔPao) obtained during simultaneous stimulation of the two phrenic nerves (measured ΔPao) to the sum of the ΔPao values produced by their separate stimulation (predicted ΔPao). The measured ΔPao was invariably greater than the predicted ΔPao, and the ratio between these two values increased gradually as the stimulation frequency was increased; the ratio was 1.10 ± 0.01 ( P < 0.05) for a frequency of 10 Hz, whereas for a frequency of 50 Hz it amounted to 1.49 ± 0.05 ( P < 0.001). This interaction remained unchanged after the rib cage was stiffened and its compliance was made linear, thus indicating that the load against which the diaphragm works is not a major determinant. However, radiographic measurements showed that stimulation of one phrenic nerve extends the inactive hemidiaphragm toward the sagittal midplane and reduces the caudal displacement of the central portion of the diaphragmatic dome. As a result, the volume swept by the contracting hemidiaphragm is smaller than the volume it displaces when the contralateral hemidiaphragm also contracts. These observations indicate that 1) the left and right hemidiaphragms have a synergistic, rather than additive, interaction on the lung; 2) this synergism operates already during quiet breathing and increases in magnitude when respiratory drive is greater; and 3) this synergism is primarily related to the configuration of the muscle.


2004 ◽  
Vol 97 (1) ◽  
pp. 85-90 ◽  
Author(s):  
Matteo Cappello ◽  
André De Troyer

The abdominal muscles expand the rib cage when they contract alone. This expansion opposes the deflation of the lung and may be viewed as pressure dissipation. The hypothesis was raised, therefore, that alterations in rib cage elastance should affect the lung deflating action of these muscles. To test this hypothesis and evaluate the quantitative importance of this effect, we measured the changes in airway opening pressure (Pao), abdominal pressure (Pab), and rib cage transverse diameter during isolated stimulation of the transversus abdominis muscle in anesthetized dogs, first with the rib cage intact and then after rib cage elastance was increased by clamping the ribs and the sternum. Stimulation produced increases in Pao, Pab, and rib cage diameter in both conditions. With the ribs and sternum clamped, however, the change in Pab was unchanged but the change in Pao was increased by 77% ( P < 0.001). In a second experiment, the transversus abdominis was stimulated before and after rib cage elastance was reduced by removing the bony ribs 3–8. Although the change in Pab after removal of the the ribs was still unchanged, the change in Pao was reduced by 62% ( P < 0.001). These observations, supported by a model analysis, indicate that rib cage elastance is a major determinant of the mechanical coupling between the abdominal muscles and the lung. In fact, in the dog, the effects of rib cage elastance and Pab on the lung-deflating action of the abdominal muscles are of the same order of magnitude.


1991 ◽  
Vol 70 (6) ◽  
pp. 2388-2394 ◽  
Author(s):  
V. Ninane ◽  
M. Gorini ◽  
M. Estenne

The action on the lung of interosseous intercostal muscles located in the third and the seventh interspaces was studied in 15 anesthetized-curarized supine dogs. Changes in pleural pressure, airflow rate, and lung volume produced by maximal stimulation of both intercostal muscle layers were measured at and above functional residual capacity (FRC). In five animals measurements were also obtained during isolated stimulation of the internal layer. At FRC, intercostal stimulation in the upper interspaces had invariably an inspiratory effect on the lung but no effect was detectable in the lower interspaces. Qualitatively similar results were obtained during isolated stimulation of the internal layer. Increasing lung volume reduced the inspiratory action of the upper intercostals and conferred an expiratory action to the lower intercostals. These results indicate the following: 1) when contracting in a single interspace, the external and internal intercostals have a qualitatively similar action on the lung; and 2) this action, however, depends critically on their location along the cephalocaudal axis of the rib cage: in the upper portion of the rib cage, both muscle layers have an inspiratory effect at and above FRC; in the lower portion of the rib cage, they have no respiratory action at FRC and act in the expiratory direction at higher lung volumes.


1993 ◽  
Vol 75 (6) ◽  
pp. 2360-2367 ◽  
Author(s):  
A. F. DiMarco ◽  
G. S. Supinski ◽  
B. Simhai ◽  
J. R. Romaniuk

The pattern of electrical activation and muscle length changes of the internal intercostal (II) muscles (9th or 10th interspace) of the lower rib cage were evaluated in supine anesthetized dogs. Studies were performed during resting breathing and expiratory threshold loading. Results were compared with simultaneous measurements of the better-studied triangularis sterni muscle (4th interspace). In general, both muscles lengthened with passive inflation and shortened with passive deflation. During resting breathing, both the II and TS muscles were electrically active and shortened below resting length, 7.7 +/- 1.6% (SE) and 5.3 +/- 1.7%, respectively. With the addition of positive end-expiratory pressure, the degree of electrical activation and muscle shortening increased progressively for both muscles, although to a somewhat greater extent for II muscles. Isolated denervation of the II muscles eliminated their shortening during resting breathing and often resulted in muscle lengthening, indicating that II muscle shortening was secondary to its own activation. Expiration was associated with lateral inward movement of the lower rib cage below its relaxation position. This motion was not significantly affected by abdominal muscle section but was markedly reduced by bilateral II denervation (7th-11th spaces). Our results indicate that the II muscles of the lower rib cage 1) are electrically active and shorten below resting length during resting breathing, 2) respond to positive end-expiratory pressure by increasing their level of activation and degree of shortening, and 3) are primarily responsible for inward lateral motion of the lower rib cage below its relaxation position during expiration.


2006 ◽  
Vol 101 (1) ◽  
pp. 169-175 ◽  
Author(s):  
André De Troyer ◽  
Dimitri Leduc

The inspiratory intercostal muscles enhance the force generated by the diaphragm during lung expansion. However, whether the diaphragm also alters the force developed by the inspiratory intercostals is unknown. Two experiments were performed in dogs to answer the question. In the first experiment, external, cranially oriented forces were applied to the different rib pairs to assess the effect of diaphragmatic contraction on the coupling between the ribs and the lung. The fall in airway opening pressure (ΔPao) produced by a given force on the ribs was invariably greater during phrenic nerve stimulation than with the diaphragm relaxed. The cranial rib displacement (Xr), however, was 40–50% smaller, thus indicating that the increase in ΔPao was exclusively the result of the increase in diaphragmatic elastance. In the second experiment, the parasternal intercostal muscle in the fourth interspace was selectively activated, and the effects of diaphragmatic contraction on the ΔPao and Xr caused by parasternal activation were compared with those observed during the application of external loads on the ribs. Stimulating the phrenic nerves increased the ΔPao and reduced the Xr produced by the parasternal intercostal, and the magnitudes of the changes were identical to those observed during external rib loading. It is concluded, therefore, that the diaphragm has no significant synergistic or antagonistic effect on the force developed by the parasternal intercostals during breathing. This lack of effect is probably related to the constraint imposed on intercostal muscle length by the ribs and sternum.


2007 ◽  
Vol 102 (2) ◽  
pp. 650-657 ◽  
Author(s):  
Dimitri Leduc ◽  
André De Troyer

Ascites, a complicating feature of many diseases of the liver and peritoneum, commonly causes dyspnea. The mechanism of this symptom, however, is uncertain. In the present study, progressively increasing ascites was induced in anesthetized dogs, and the hypothesis was initially tested that ascites increases the impedance on the diaphragm and, so, adversely affects the lung-expanding action of the muscle. Ascites produced a gradual increase in abdominal elastance and an expansion of the lower rib cage. Concomitantly, the caudal displacement of the diaphragm and the fall in airway opening pressure during isolated stimulation of the phrenic nerves decreased markedly; transdiaphragmatic pressure during phrenic stimulation also decreased. To assess the adaptation to ascites of the respiratory system overall, we subsequently measured the changes in lung volume, the arterial blood gases, and the electromyogram of the parasternal intercostal muscles during spontaneous breathing. Tidal volume and minute ventilation decreased progressively as ascites increased, leading to an increase in arterial Pco2 and parasternal intercostal inspiratory activity. It is concluded that 1) ascites, acting through an increase in abdominal elastance and an expansion of the lower rib cage, impairs the lung-expanding action of the diaphragm; 2) this impairment elicits a compensatory increase in neural drive to the inspiratory muscles, but the compensation is not sufficient to maintain ventilation; and 3) dyspnea in this setting results in part from the dissociation between increased neural drive and decreased ventilation.


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