Effect of diaphragmatic contraction on the action of the canine parasternal intercostals

2006 ◽  
Vol 101 (1) ◽  
pp. 169-175 ◽  
Author(s):  
André De Troyer ◽  
Dimitri Leduc
Keyword(s):  
Nerve Stimulation ◽  
Muscle Length ◽  
Antagonistic Effect ◽  
Intercostal Muscle ◽  
Phrenic Nerve Stimulation ◽  
Opening Pressure ◽  
Lung Expansion ◽  
Airway Opening ◽  
Phrenic Nerves ◽  
External Loads

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.

The action of the canine diaphragm on the lower ribs depends on activation

2011 ◽  
Vol 111 (5) ◽  
pp. 1266-1271 ◽  
Author(s):  
André De Troyer
Keyword(s):  
Nerve Stimulation ◽  
Phrenic Nerve ◽  
Muscle Activation ◽  
Pleural Pressure ◽  
Phrenic Nerve Stimulation ◽  
Nerve Roots ◽  
Neural Drive ◽  
Airway Opening ◽  
Phrenic Nerves ◽  
Spontaneously Breathing

Conventional wisdom maintains that the diaphragm lifts the lower ribs during isolated contraction. Recent studies in dogs have shown, however, that supramaximal, tetanic stimulation of the phrenic nerves displaces the lower ribs caudally and inward. In the present study, the hypothesis was tested that the action of the canine diaphragm on these ribs depends on the magnitude of muscle activation. Two experiments were performed. In the first, the C5 and C6 phrenic nerve roots were selectively stimulated in 6 animals with the airway occluded, and the level of diaphragm activation was altered by adjusting the stimulation frequency. In the second experiment, all the inspiratory intercostal muscles were severed in 7 spontaneously breathing animals, so that the diaphragm was the only muscle active during inspiration, and neural drive was increased by a succession of occluded breaths. The changes in airway opening pressure and the craniocaudal displacements of ribs 5 and 10 were measured in each animal. The data showed that 1) contraction of the diaphragm causes the upper ribs to move caudally; 2) during phrenic nerve stimulation, the lower ribs move cranially when the level of diaphragm activation is low, but they move caudally when the level of muscle activation is high and the entire rib cage is exposed to pleural pressure; and 3) during spontaneous diaphragm contraction, however, the lower ribs always move cranially, even when neural drive is elevated and the change in pleural pressure is large. It is concluded that the action of the diaphragm on the lower ribs depends on both the magnitude and the mode of muscle activation. These findings can reasonably explain the apparent discrepancies between previous studies. They also imply that observations made during phrenic nerve stimulation do not necessarily reflect the physiological action of the diaphragm.

Role of the mediastinum in the mechanics of the canine diaphragm

2010 ◽  
Vol 109 (1) ◽  
pp. 27-34 ◽  
Author(s):  
André De Troyer ◽  
Matteo Cappello ◽  
Dimitri Leduc ◽  
Pierre Alain Gevenois
Keyword(s):  
Nerve Stimulation ◽  
Phrenic Nerve ◽  
Three Dimensional ◽  
Vena Cava ◽  
Muscle Length ◽  
Phrenic Nerve Stimulation ◽  
Lung Volumes ◽  
Airway Opening ◽  
Generating Capacity

The objective of this study was to evaluate the role of the mediastinum in the mechanics of the canine diaphragm. Two sets of experiments were performed. In the first experiment on five animals, the mediastinum was severed from the sternum to the vena cava, and radiopaque markers were attached to muscle bundles in the midcostal region of the diaphragm. The three-dimensional location of the markers during relaxation at different lung volumes and during phrenic nerve stimulation at the same lung volumes was then measured using computed tomography. From these data, accurate measurements of muscle displacement and muscle length were obtained, and these measurements, together with the changes in airway opening pressure, were compared with those previously obtained in animals with an intact mediastinum. Severing the mediastinum per se appeared to have no influence on the pressure-generating capacity of the diaphragm or on the lung-volume dependence of this capacity. The great vessels and the esophagus in these animals, however, were left intact, so the possibility remained that these structures continued to impact on the diaphragm through their close attachments to the muscle. In the second experiment, therefore, loads were applied caudally to the central tendon to assess the force-displacement relationship of the entire mediastinum, and this relationship, combined with the known displacement of the diaphragm dome during phrenic nerve stimulation, was used to infer the force exerted by the mediastinum on the muscle during contraction. The results showed that this force is small compared with that developed by the diaphragm, except at very high lung volumes. It is concluded, therefore, that the mediastinum has only little influence on the mechanics of the canine diaphragm.

Mechanism of the lung-deflating action of the canine diaphragm at extreme lung inflation

2012 ◽  
Vol 112 (8) ◽  
pp. 1311-1316 ◽  
Author(s):  
Dimitri Leduc ◽  
Matteo Cappello ◽  
Pierre Alain Gevenois ◽  
André De Troyer
Keyword(s):  
Nerve Stimulation ◽  
Phrenic Nerve ◽  
Pleural Pressure ◽  
Phrenic Nerve Stimulation ◽  
Lung Volumes ◽  
Lung Inflation ◽  
Lower Lung ◽  
Airway Opening ◽  
Radiopaque Markers ◽  
Phrenic Nerves

When lung volume in animals is passively increased beyond total lung capacity (TLC; transrespiratory pressure = +30 cmH2O), stimulation of the phrenic nerves causes a rise, rather than a fall, in pleural pressure. It has been suggested that this was the result of inward displacement of the lower ribs, but the mechanism is uncertain. In the present study, radiopaque markers were attached to muscle bundles in the midcostal region of the diaphragm and to the tenth rib pair in five dogs, and computed tomography was used to measure the displacement, length, and configuration of the muscle and the displacement of the lower ribs during relaxation at seven different lung volumes up to +60 cmH2O transrespiratory pressure and during phrenic nerve stimulation at the same lung volumes. The data showed that 1) during phrenic nerve stimulation at 60 cmH2O, airway opening pressure increased by 1.5 ± 0.7 cmH2O; 2) the dome of the diaphragm and the lower ribs were essentially stationary during such stimulation, but the muscle fibers still shortened significantly; 3) with passive inflation beyond TLC, an area with a cranial concavity appeared at the periphery of the costal portion of the diaphragm, forming a groove along the ventral third of the rib cage; and 4) this area decreased markedly in size or disappeared during phrenic stimulation. It is concluded that the lung-deflating action of the isolated diaphragm beyond TLC is primarily related to the invaginations in the muscle caused by the acute margins of the lower lung lobes. These findings also suggest that the inspiratory inward displacement of the lower ribs commonly observed in patients with emphysema (Hoover's sign) requires not only a marked hyperinflation but also a large fall in pleural pressure.

Validation of improved recording site to measure phrenic conduction from surface electrodes in humans

2002 ◽  
Vol 92 (3) ◽  
pp. 967-974 ◽  
Author(s):  
Eric Verin ◽  
Christian Straus ◽  
Alexandre Demoule ◽  
Philippe Mialon ◽  
Jean-Philippe Derenne ◽  
...  
Keyword(s):  
Nerve Stimulation ◽  
Phrenic Nerve ◽  
Magnetic Stimulation ◽  
Conduction Time ◽  
Phrenic Nerve Stimulation ◽  
Recording Site ◽  
Serratus Anterior ◽  
Surface Electrodes ◽  
Phrenic Nerves

Phrenic nerve stimulation, electrical (ES) or from cervical magnetic stimulation (CMS), allows one to assess the diaphragm contractile properties and the conduction time of the phrenic nerve (PNCT) through recording of an electromyographic response, traditionally by using surface electrodes. Because of the coactivation of extradiaphragmatic muscles, signal contamination can jeopardize the determination of surface PNCTs. To address this, we compared PNCTs with ES and CMS from surface and needle diaphragm electrodes in five subjects (10 phrenic nerves). At a modified recording site, lower and more anterior than usual (lowest accessible intercostal space, costochondral junction) with electrodes 2 cm apart, surface and needle PNCTs were similar (CMS: 6.0 ± 0.25 ms surface vs. 6.2 ± 0.13 ms needle, not significant). Electrodes recording the activity of the most likely sources of signal contamination, i.e., the serratus anterior and pectoralis major, showed distinct responses from that of the diaphragm, their earlier occurrence strongly arguing against contamination. With ES and CMS, apparently uncontaminated signals could be consistently recorded from surface electrodes.

The two mechanisms of intercostal muscle action on the lung

2004 ◽  
Vol 96 (2) ◽  
pp. 483-488 ◽  
Author(s):  
Theodore A. Wilson ◽  
Andre De Troyer
Keyword(s):  
Three Dimensional ◽  
Intercostal Muscle ◽  
Muscle Action ◽  
Opening Pressure ◽  
Rib Cage ◽  
Intercostal Muscles ◽  
Airway Opening ◽  
The Difference ◽  
External Forces

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.

The effect of lung inflation on the inspiratory action of the canine parasternal intercostals

2006 ◽  
Vol 100 (3) ◽  
pp. 858-863 ◽  
Author(s):  
Dimitri Leduc ◽  
André De Troyer
Keyword(s):  
Functional Residual Capacity ◽  
Negative Impact ◽  
Chronic Obstructive ◽  
Electromyographic Activity ◽  
Opening Pressure ◽  
Obstructive Pulmonary Disease ◽  
Lung Inflation ◽  
Airway Opening ◽  
Residual Capacity ◽  
Phrenic Nerves

Inflation induces a marked decrease in the lung-expanding ability of the diaphragm, but its effect on the parasternal intercostal muscles is uncertain. To assess this effect, the phrenic nerves and the external intercostals were severed in anesthetized, vagotomized dogs, such that the parasternal intercostals were the only muscles active during inspiration, and the endotracheal tube was occluded at different lung volumes. Although the inspiratory electromyographic activity recorded from the muscles was constant, the change in airway opening pressure decreased with inflation from −7.2 ± 0.6 cmH2O at functional residual capacity to −2.2 ± 0.2 cmH2O at 20-cmH2O transrespiratory pressure ( P < 0.001). The inspiratory cranial displacement of the ribs remained virtually unchanged, and the inspiratory caudal displacement of the sternum decreased moderately. However, the inspiratory outward rib displacement decreased markedly and continuously; at 20 cmH2O, this displacement was only 23 ± 2% of the value at functional residual capacity. Calculations based on this alteration yielded substantial decreases in the change in airway opening pressure. It is concluded that, in the dog, 1) inflation affects adversely the lung-expanding actions of both the parasternal intercostals and the diaphragm; and 2) the adverse effect of inflation on the parasternal intercostals is primarily related to the alteration in the kinematics of the ribs. As a corollary, it is likely that hyperinflation also has a negative impact on the parasternal intercostals in patients with chronic obstructive pulmonary disease.

scholarly journals Length and curvature of the dog diaphragm

2006 ◽  
Vol 101 (3) ◽  
pp. 794-798 ◽  
Author(s):  
Aladin M. Boriek ◽  
Ben Black ◽  
Rolf Hubmayr ◽  
Theodore A. Wilson
Keyword(s):  
Nerve Stimulation ◽  
Phrenic Nerve ◽  
Muscle Length ◽  
Lung Compliance ◽  
Chronic Obstructive ◽  
Phrenic Nerve Stimulation ◽  
Lung Volumes ◽  
Obstructive Pulmonary Disease ◽  
Transdiaphragmatic Pressure ◽  
Residual Capacity

Transdiaphragmatic pressure is a result of both tension in the muscles of the diaphragm and curvature of the muscles. As lung volume increases, the pressure-generating capability of the diaphragm decreases. Whether decrease in curvature contributes to the loss in transdiaphragmatic pressure and, if so, under what conditions it contributes are unknown. Here we report data on muscle length and curvature in the supine dog. Radiopaque markers were attached along muscle bundles in the midcostal region of the diaphragm in six beagle dogs of ∼8 kg, and marker locations were obtained from biplanar images at functional residual capacity (FRC), during spontaneous inspiratory efforts against a closed airway at lung volumes from FRC to total lung capacity, and during bilateral maximal phrenic nerve stimulation at the same lung volumes. Muscle length and curvature were obtained from these data. During spontaneous inspiratory efforts, muscle shortened by 15–40% of length at FRC, but curvature remained unchanged. During phrenic nerve stimulation, muscle shortened by 30 to nearly 50%, and, for shortening exceeding 52%, curvature appeared to decrease sharply. We conclude that diaphragm curvature is nearly constant during spontaneous breathing maneuvers in normal animals. However, we speculate that it is possible, if lung compliance were increased and the chest wall and the diameter of the diaphragm ring of insertion were enlarged, as in the case of chronic obstructive pulmonary disease, that decrease in diaphragm curvature could contribute to loss of diaphragm function.

Mechanics of the canine diaphragm in ascites: a CT study

2008 ◽  
Vol 104 (2) ◽  
pp. 423-428 ◽  
Author(s):  
Dimitri Leduc ◽  
Matteo Cappello ◽  
Pierre Alain Gevenois ◽  
André De Troyer
Keyword(s):  
Nerve Stimulation ◽  
Phrenic Nerve ◽  
Three Dimensional ◽  
Muscle Length ◽  
Phrenic Nerve Stimulation ◽  
Additional Increase ◽  
Transdiaphragmatic Pressure ◽  
Computed Tomographic ◽  
Muscle Shortening ◽  
Radiopaque Markers

Ascites causes an increase in the elastance of the abdomen and impairs the lung-expanding action of the diaphragm, but its overall effects on the pressure-generating ability of the muscle remain unclear. In the present study, radiopaque markers were attached to muscle bundles in the midcostal region of the diaphragm in five dogs, and the three-dimensional locations of the markers during relaxation and during phrenic nerve stimulation in the presence of increasing amounts of ascites were determined using a computed tomographic scanner. From these data, accurate measurements of muscle length and quantitative estimates of diaphragm curvature were obtained, and the changes in transdiaphragmatic pressure (Pdi) were analyzed as functions of muscle length and curvature. With increasing ascites, the resting length of the diaphragm increased progressively. In addition, the amount of muscle shortening during phrenic nerve stimulation decreased gradually. When ascites was 100 ml/kg body wt, therefore, the muscle during contraction was longer, leading to a 20–25% increase in Pdi. As ascites increased further to 200 ml/kg, however, muscle length during contraction continued to increase, but Pdi did not. This absence of additional increase in Pdi was well explained by the increase in the diameter of the ring of insertion of the diaphragm to the rib cage and the concomitant increase in the radius of diaphragm curvature. These observations indicate that the pressure-generating ability of the diaphragm is determined not only by muscle length as conventionally thought but also by muscle shape.

scholarly journals Impact of diaphragmatic contraction on the stiffness of the canine mediastinum

2008 ◽  
Vol 105 (3) ◽  
pp. 887-893 ◽  
Author(s):  
André De Troyer
Keyword(s):  
Opening Pressure ◽  
Ipsilateral Lung ◽  
Contralateral Lung ◽  
Pressure Transmission ◽  
Airway Opening ◽  
Anesthetized Dogs ◽  
Phrenic Nerves ◽  
Left And Right ◽  
The Mean ◽  
The Individual

To assess the coupling between a particular hemidiaphragm and the individual lungs, the left and right phrenic nerves were separately stimulated in anesthetized dogs, and the mean changes in pleural pressure over the two lungs were evaluated by measuring the changes in airway opening pressure (ΔPao) in the two bronchial trees. Stimulation induced a fall in Pao in both lungs. However, ΔPao in the contralateral lung was only 65% of that in the ipsilateral lung. Thus, although the canine ventral mediastinum is a delicate structure, it sustained a significant pressure gradient. The hypothesis was then considered that this gradient was allowed to develop through the stretching and stiffening of the mediastinum caused by the descent of the diaphragm, and it was tested by measuring ΔPao in the two lungs during isolated, unilateral contraction of the inspiratory intercostal muscles. In this condition, ΔPao in the contralateral lung was 92% of that in the ipsilateral lung. A model analysis of the respiratory system led to the estimate that mediastinal elastance was ∼25 times greater during hemidiaphragmatic contraction than during unilateral intercostal contraction. These observations indicate that 1) a particular hemidiaphragm has an expanding action on both lungs and 2) during contraction, however, it makes the mediastinum stiffer so that the pressure transmission from the ipsilateral to the contralateral pleural cavity is reduced. These observations imply that the mediastinum may play a significant role in determining the pressure-generating ability of the diaphragm.

Mediolateral gradient of mechanical advantage in the canine parasternal intercostals

1996 ◽  
Vol 80 (6) ◽  
pp. 2097-2101 ◽  
Author(s):  
A. Legrand ◽  
T. A. Wilson ◽  
A. D. Troyer
Keyword(s):  
Respiratory Muscles ◽  
Potential Effect ◽  
Intercostal Nerve ◽  
Opening Pressure ◽  
Respiratory Effect ◽  
Lung Expansion ◽  
Airway Opening ◽  
Anesthetized Dogs ◽  
Lateral Portion ◽  
Stimulation Of

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.

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