Publications by authors named "Andre De Troyer"

When the diaphragm contracts, pleural pressure falls, exerting a caudal and inward force on the entire rib cage. However, the diaphragm also exerts forces in the cranial and outward direction on the lower ribs. One of these forces, the "insertional force," is applied by the muscle at its attachments to the lower ribs.

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When the abdomen in quadriplegic subjects is given a passive mechanical support, the expansion of the lower rib cage during inspiration is greater and the inward displacement of the upper rib cage is smaller. These changes have traditionally been attributed to an increase in the appositional force of the diaphragm, but the mechanisms have not been assessed. In this study, the inspiratory intercostal muscles in all interspaces were severed in anesthetized dogs, so that the diaphragm was the only muscle active during inspiration, and the displacements of the ribs 10 and 5 and the changes in pleural and abdominal pressure were measured during unimpeded breathing and during breathing with a plate applied on the ventral abdominal wall.

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The normal diaphragm has an inspiratory action on the lower ribs, but subjects with chronic obstructive pulmonary disease commonly have an inward displacement of the lateral portions of the lower rib cage during inspiration. This paradoxical displacement, conventionally called 'Hoover's sign', has traditionally been attributed to the direct action of radially oriented diaphragmatic muscle fibres. In the present study, the inspiratory intercostal muscles in all interspaces in anaesthetized dogs were severed so that the diaphragm was the only muscle active during inspiration.

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The diaphragm has an inspiratory action on the lower ribs, and current conventional wisdom maintains that this action is the result of two mechanisms, namely, the force applied by the muscle fibres on the ribs into which they insert (insertional force) and the transmission of abdominal pressure through the zone of apposition (appositional force). The magnitude of the diaphragmatic force and the relative contributions of the insertional and appositional components, however, are unknown. To assess these forces, the inspiratory intercostal muscles in all interspaces were severed in anaesthetized dogs, so that the diaphragm was the only muscle active during inspiration, and the displacements of the lower ribs along the craniocaudal and laterolateral axes were measured during quiet breathing, during occluded breaths and during passive lung inflation.

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Pleural effusion, a complicating feature of many diseases of the lung and pleura, adversely affects the pressure-generating capacity of the diaphragm in supine dogs. The objective of the present study was to assess the impact of body position on this effect and to evaluate the adaptation to effusion of the inspiratory muscle pump during breathing. Two experiments were performed.

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Pleural effusion is a complicating feature of many diseases of the lung and pleura, but its effects on the mechanics of the diaphragm have not been assessed. In the present study, radiopaque markers were attached along muscle bundles in the midcostal region of the diaphragm in anesthetized dogs, and the three-dimensional location of the markers during relaxation before and after the stepwise introduction of liquid into the left or right pleural space and during phrenic nerve stimulation in the same conditions was determined using computed tomography. From these data, accurate measurements of diaphragm muscle length and displacement were obtained, and the changes in pleural and abdominal pressure were analyzed as functions of these parameters.

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When lung volume in animals is passively increased beyond total lung capacity (TLC; transrespiratory pressure = +30 cmH(2)O), 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 cmH(2)O transrespiratory pressure and during phrenic nerve stimulation at the same lung volumes.

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The diaphragm acting alone causes a cranial displacement of the lower ribs and a caudal displacement of the upper ribs. The respiratory effect of the lower rib displacement, however, is uncertain. In the present study, two sets of experiments were performed in dogs to assess this effect.

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The objectives of the present study were to test the hypothesis that the costal diaphragm contracts during ipsilateral rotation of the trunk and that such trunk rotation increases the motor output of the muscle during inspiration. Monopolar electrodes were inserted in the right costal hemidiaphragm in six subjects, and electromyographic (EMG) recordings were made during isometric rotation efforts of the trunk to the right ("ipsilateral rotation") and to the left ("contralateral rotation"). EMG activity was simultaneously recorded from the parasternal intercostal muscles on the right side.

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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.

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This article examines the mechanics of the muscles that drive expansion or contraction of the chest wall during breathing. The diaphragm is the main inspiratory muscle. When its muscle fibers are activated in isolation, they shorten, the dome of the diaphragm descends, pleural pressure (P(pl)) falls, and abdominal pressure (P(ab)) rises.

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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.

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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.

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The parasternal intercostal muscles are obligatory inspiratory muscles. To test the hypothesis that they are also involved in trunk rotation and to assess the effect of any postural role on inspiratory drive to the muscles, intramuscular electromyographic (EMG) recordings were made from the parasternal intercostals on the right side in six healthy subjects during resting breathing in a neutral posture ("neutral breaths"), during an isometric axial rotation effort of the trunk to the right ("ipsilateral rotation") or left ("contralateral rotation"), and during resting breathing with the trunk rotated. The parasternal intercostals were commonly active during ipsilateral rotation but were consistently silent during contralateral rotation.

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During isolated phrenic nerve stimulation, the muscles of the diaphragm shorten by 40-50% of their optimal length, and the force in the muscle and transdiaphragmatic pressure (Pdi) depend on the final muscle length. The muscle shortening depends on the load imposed on the diaphragm by pleural and abdominal pressures during a particular maneuver. The mechanics of the interaction between the diaphragm and the load is well understood, but the force-length properties of the diaphragm are nonlinear, and an algebraic analysis of the interaction is clumsy.

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The lung-expanding action of the diaphragm is primarily related to the descent of the dome produced by the shortening of the muscle fibers. However, when the phrenic nerves in dogs are selectively stimulated at functional residual capacity, the muscle insertions into the lower ribs also move caudally. This rib motion should enhance the descent of the dome and increase the fall in pleural pressure (DeltaPpl).

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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 (X(r)) in the control condition and caused a cranial rib displacement in the presence of ascites.

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The present study was designed to test the hypothesis that the expansion of a particular lung during breathing is partly related to the action of the hemidiaphragm on the opposite side. Two endotracheal tubes were inserted in the right and left main stem bronchi of anesthetized dogs, and the changes in pleural pressure (DeltaPpl) over the two lungs were assessed separately, first before and then after section of one phrenic nerve, by measuring the changes in airway opening pressure (DeltaPao) in the two tubes during occluded breaths. After phrenic nerve section, DeltaPao in the ipsilateral lung decreased 28+/-2%, and DeltaPao in the contralateral lung decreased 16+/-2% (P<0.

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When the lung is inflated acutely, the capacity of the diaphragm to generate pressure, in particular pleural pressure (Ppl), is impaired because the muscle during contraction is shorter and generates less force. At very high lung volumes, the pressure-generating capacity of the diaphragm may be further reduced by an increase in the muscle radius of curvature. Lung inflation similarly impairs the pressure-generating capacity of the inspiratory intercostal muscles, both the parasternal intercostals and the external intercostals.

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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 (DeltaPao) in the two bronchial trees. Stimulation induced a fall in Pao in both lungs. However, DeltaPao in the contralateral lung was only 65% of that in the ipsilateral lung.

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Although ascites causes abdominal expansion, its effects on abdominal muscle function are uncertain. In the present study, progressively increasing ascites was induced in supine anesthetized dogs, and the changes in abdominal (DeltaPab) and airway opening (DeltaPao) pressure obtained during stimulation of the internal oblique and transversus abdominis muscles were measured; the changes in internal oblique muscle length were also measured. As ascites increased from 0 to 100 ml/kg body wt, Pab and muscle length during relaxation increased.

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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.

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The inspiratory intercostal muscles elevate the ribs and thereby elicit a fall in pleural pressure (DeltaPpl) when they contract. In the present study, we initially tested the hypothesis that this DeltaPpl does, in turn, oppose the rib elevation. The cranial rib displacement (Xr) produced by selective activation of the parasternal intercostal muscle in the fourth interspace was measured in dogs, first with the rib cage intact and then after DeltaPpl was eliminated by bilateral pneumothorax.

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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.

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