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.

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.

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.

scholarly journals Diaphragm curvature modulates the relationship between muscle shortening and volume displacement

2011 ◽  
Vol 301 (1) ◽  
pp. R76-R82 ◽  
Author(s):  
Brad J. Greybeck ◽  
Matthew Wettergreen ◽  
Rolf D. Hubmayr ◽  
Aladin M. Boriek
Keyword(s):  
Nerve Stimulation ◽  
Phrenic Nerve ◽  
Spontaneous Breathing ◽  
Three Dimensional ◽  
Diaphragm Muscle ◽  
Phrenic Nerve Stimulation ◽  
Lung Volumes ◽  
Muscle Shortening ◽  
Residual Capacity ◽  
The Relationship

During physiological spontaneous breathing maneuvers, the diaphragm displaces volume while maintaining curvature. However, with maximal diaphragm activation, curvature decreases sharply. We tested the hypotheses that the relationship between diaphragm muscle shortening and volume displacement (VD) is nonlinear and that curvature is a determinant of such a relationship. Radiopaque markers were surgically placed on three neighboring muscle fibers in the midcostal region of the diaphragm in six dogs. The three-dimensional locations were determined using biplanar fluoroscopy and diaphragm VD, curvature, and muscle shortening were computed in the prone and supine postures during spontaneous breathing (SB), spontaneous inspiration efforts after airway occlusion at lung volumes ranging from functional residual capacity (FRC) to total lung capacity, and during bilateral maximal phrenic nerve stimulation at those same lung volumes. In supine dogs, diaphragm VD was approximately two- to three-fold greater during maximal phrenic nerve stimulation than during SB. The contribution of muscle shortening to VD nonlinearly increases with level of diaphragm activation independent of posture. During submaximal diaphragm activation, the contribution is essentially linear due to constancy of diaphragm curvature in both the prone and supine posture. However, the sudden loss of curvature during maximal bilateral phrenic nerve stimulation at muscle shortening values greater than 40% (ΔL/LFRC) causes a nonlinear increase in the contribution of muscle shortening to diaphragm VD, which is concomitant with a nonlinear change in diaphragm curvature. We conclude that the nonlinear relationship between diaphragm muscle shortening and its VD is, in part, due to a loss of its curvature at extreme muscle shortening.

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.

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.

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.

Effect of lung volume on in vivo contraction characteristics of human diaphragm

1987 ◽  
Vol 62 (5) ◽  
pp. 1893-1900 ◽  
Author(s):  
J. Smith ◽  
F. Bellemare
Keyword(s):  
Nerve Stimulation ◽  
Lung Volume ◽  
Phrenic Nerve ◽  
Pleural Pressure ◽  
Normal Male ◽  
Contraction Time ◽  
Phrenic Nerve Stimulation ◽  
Transdiaphragmatic Pressure ◽  
Gastric Pressure

We performed transcutaneous bilateral phrenic nerve stimulation at varying lung volumes between residual volume (RV) and total lung capacity (TLC) in six normal male volunteers. Peak twitch transdiaphragmatic pressure declined from 49.1 +/- 9.1 (SD) cmH2O at RV to 19.6 +/- 5.97 (SD) cmH2O at TLC. Twitch contraction time fell from 91.8 +/- 11.3 (SD) ms at RV to 57.7 +/- 7.4 (SD) ms at TLC. There was a good correlation between changes in contraction time and transdiaphragmatic pressure (r = 0.7). The fall in transdiaphragmatic pressure was almost all due to a fall in pleural pressure, with little change in gastric pressure between RV and TLC. At TLC the pleural pressure in response to phrenic nerve stimulation was -0.58 cmH2O. We conclude that, as lung volume increases and the diaphragm shortens, it becomes less effective as a pressure generator and that pressure it generates is less well converted into useful inspiratory pressure. At a lung volume close to TLC, the diaphragm ceases to act as an inspiratory muscle.

Asymmetrical action of the canine diaphragm after single-lung inflation

2011 ◽  
Vol 110 (6) ◽  
pp. 1519-1525 ◽  
Author(s):  
André De Troyer ◽  
Dimitri Leduc ◽  
Pierre Alain Gevenois ◽  
Matteo Cappello
Keyword(s):  
Radius Of Curvature ◽  
Lung Inflation ◽  
Endotracheal Tubes ◽  
Computed Tomographic ◽  
Airway Opening ◽  
Anesthetized Dogs ◽  
Radiopaque Markers ◽  
Phrenic Nerves ◽  
The Right ◽  
Phrenic Stimulation

Single-lung transplantation (SLT) in patients with emphysema leads to a cranial displacement of the diaphragm on the transplanted side and a shift of the mediastinum toward the transplanted lung. The objective of the present study was to assess the effect of unilateral lung inflation on the mechanics of the diaphragm. Two endotracheal tubes were inserted in the two main stem bronchi of six anesthetized dogs, and radiopaque markers were attached along muscle fibers in the midcostal region of the two halves of the diaphragm. The animals were then placed in a computed tomographic scanner, the left or the right lung was passively inflated, and the phrenic nerves were stimulated while the two endobronchial tubes were occluded. As lung volume increased, the fall in airway opening pressure (ΔPao) in the inflated lung during stimulation decreased markedly, whereas ΔPao in the noninflated lung decreased only moderately ( P < 0.001). Also, the two hemidiaphragms shortened both during relaxation and during phrenic stimulation, but the ipsilateral hemidiaphragm was consistently shorter than the contralateral hemidiaphragm. In addition, the radius of curvature of the ipsilateral hemidiaphragm during stimulation increased, whereas the radius of the contralateral hemidiaphragm remained unchanged. These observations indicate that 1) in the presence of unilateral lung inflation, the respiratory action of the diaphragm is asymmetric; and 2) this asymmetry is primarily determined by the differential effect of inflation on the length and curvature of the two halves of the muscle. These observations also imply that in patients with emphysema, SLT improves the action of the diaphragm on the transplanted side.

scholarly journals Mechanism of increased inspiratory rib elevation in ascites

2009 ◽  
Vol 107 (3) ◽  
pp. 734-740 ◽  
Author(s):  
Dimitri Leduc ◽  
André De Troyer
Keyword(s):  
Nerve Stimulation ◽  
Phrenic Nerve ◽  
Detrimental Effect ◽  
Muscle Force ◽  
Intercostal Muscle ◽  
Phrenic Nerve Stimulation ◽  
Lung Inflation ◽  
Rib Cage ◽  
Pressure Swing

The detrimental effect of ascites on the lung-expanding action of the diaphragm is partly compensated for by an increase in the inspiratory elevation of the ribs, but the mechanism of this increase is uncertain. To identify this mechanism, the effect of ascites on the response of rib 4 to isolated phrenic nerve stimulation was first assessed in four dogs with bilateral pneumothoraces. Stimulation did not produce any axial displacement of the rib ( Xr) in the control condition and caused a cranial rib displacement in the presence of ascites. This displacement, however, was small. In a second experiment, the effects of ascites on the pleural pressure swing (ΔPpl), intercostal activity, and Xr during spontaneous inspiration were measured in eight animals. As the volume of ascites increased from 0 to 200 ml/kg body wt, Xr increased from 3.5 ± 0.5 to 7.5 ± 0.9 mm ( P < 0.001), ΔPpl decreased from −6.4 ± 0.4 to −3.6 ± 0.3 cmH20 ( P < 0.001), and parasternal intercostal activity increased 61 ± 19% ( P < 0.001). The role of the decrease in ΔPpl in causing the increase in Xr was then separated from that of the increase in intercostal muscle force using the relation between Xr and ΔPpl during passive lung inflation. The loss in ΔPpl accounted for two-thirds of the increase in Xr. These observations indicate that 1) the increased inspiratory elevation of the ribs in ascites is not the result of the increase in the rib cage-expanding action of the diaphragm and 2) it is due mostly to the decrease in ΔPpl and partly to the increase in the force exerted by the parasternal intercostals on the ribs. These observations also suggest, however, that the rib cage expansion caused by ascites makes the parasternal intercostals less effective in pulling the ribs cranially.

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